bluuebunny/crossref_metadata_2025_split huggingface dataset:
Fusarium spp. associated with rice Bakanae: ecology, genetic diversity, pathogenicity and toxigenicity
Authors: Wulff Ednar G. , Sørensen Jens L. , Lübeck Mette , Nielsen Kristian F. , Thrane Ulf , Torp Jan 
Published: November 2009

SummaryAfrican and Asian populations of Fusarium spp. (Gibberella fujikuroi species complex) associated with Bakanae of rice (Oryzae sativa L.) were isolated from seeds and characterized with respect to ecology, phylogenetics, pathogenicity and mycotoxin production. Independent of the origin, Fusarium spp. were detected in the different rice seed samples with infection rate ranges that varied from 0.25% to 9%. Four Fusaria (F. andiyazi, F. fujikuroi, F. proliferatum and F. verticillioides) were found associated with Bakanae of rice. While three of the Fusaria were found in both African and Asian seed samples, F. fujikuroi was only detected in seed samples from Asia. Phylogenetic studies showed a broad genetic variation among the strains that were distributed into four different genetic clades. Pathogenicity tests showed that all strains reduced seed germination and possessed varying ability to cause symptoms of Bakanae on rice, some species (i.e. F. fujikuroi) being more pathogenic than others. The ability to produce fumonisins (FB1 and FB2) and gibberellin A3 in vitro also differed according to the Fusarium species. While fumonisins were produced by most of the strains of F. verticillioides and F. proliferatum, gibberellin A3 was only produced by F. fujikuroi. Neither fumonisin nor gibberellin was synthesized by most of the strains of F. andiyazi. These findings provide new information on the variation within the G. fujikuroi species complex associated with rice seed and Bakanae disease.
Anthropogenic disturbance affects the structure of bacterial communities
Authors: Ager Duane , Evans Simon , Li Hong , Lilley Andrew K. , Van Der Gast Christopher J. 
Published: November 2009

SummaryPatterns of taxa abundance distributions are the result of the combined effects of historical and biological processes and as such are central to ecology. It is accepted that a taxa abundance distribution for a given community of animals or plants following a perturbation will typically change in structure from one of high evenness to increasing dominance. Subsequently, such changes in evenness have been used as indicators of biological integrity and environmental assessment. Here, using replicated experimental treehole microcosms perturbed with different concentrations of the pollutant pentachlorophenol, we investigated whether changes in bacterial community structure would reflect the effects of anthropogenic stress in a similar manner to larger organisms. Community structure was visualized using rank–abundance plots fitted with linear regression models. The slopes of the regression models were used as a descriptive statistic of changes in evenness over time. Our findings showed that bacterial community structure reflected the impact and the recovery from an anthropogenic disturbance. In addition, the intensity of impact and the rate of recovery to pre‐perturbation structure were dose‐dependent. These properties of bacterial community structures may potentially provide a metric for environmental assessment and regulation.
Abundances of crenarchaeal amoA genes and transcripts in the Pacific Ocean
Authors: Church Matthew J. , Wai Brenner , Karl David M. , DeLong Edward F. 
Published: November 2009

SummaryPlanktonic Crenarchaea are thought to play a key role in chemolithotrophic ammonia oxidation, a critical step of the marine nitrogen (N) cycle. In this study, we examined the spatial distributions of ammonia‐oxidizing Crenarchaea across a large (∼5200 km) region of the central Pacific Ocean. Examination of crenarchaeal 16S rRNA, ammonia monooxygenase subunit A (amoA) genes, and amoA transcript abundances provided insight into their spatial distributions and activities. Crenarchaeal gene abundances increased three to four orders of magnitude with depth between the upper ocean waters and dimly lit waters of the mesopelagic zone. The resulting median value of the crenarchaeal amoA: 16S rRNA gene ratio was 1.3, suggesting the majority of Crenarchaea in the epi‐ and mesopelagic regions of the Pacific Ocean have the metabolic machinery for ammonia oxidation. Crenarchaeal amoA transcript abundances typically increased one to two orders of magnitude in the transitional zone separating the epipelagic waters from the mesopelagic (100–200 m), before decreasing into the interior of the mesopelagic zone. The resulting gene copy normalized transcript abundances revealed elevated amoA expression in the upper ocean waters (0–100 m) where crenarchaeal abundances were low, with transcripts decreasing into the mesopelagic zone as crenarchaeal gene abundances increased. These results suggest ammonia‐oxidizing Crenarchaea are active contributors to the N cycle throughout the epi‐ and mesopelagic waters of the Pacific Ocean.
Genetic analyses ofPseudomonas aeruginosaisolated from healthy captive snakes: evidence of high inter‐ and intrasite dissemination and occurrence of antibiotic resistance genes
Authors: Colinon Céline , Jocktane Dominique , Brothier Elisabeth , Rossolini Gian Maria , Cournoyer Benoit , Nazaret Sylvie 
Published: November 2009

SummaryFaecal carriage ofPseudomonas aeruginosawas investigated by selective plating and PCR identification test, among healthy captive snakes from zoological and private collections from France as well as from wild snakes from Guinea.P. aeruginosafaecal carriage among captive snakes was high (72 out of 83 individuals), but low among wild specimen (3 out of 23 individuals). Genetic diversity analyses of the isolates, based on SpeI‐PFGE profiles, evidenced five dominant clones or clonal complexes spreading among snakes within a site and between sites and persisting over time. Similar clones or clonal complexes were detected from mouth swabs of the owners and from water and preys used to feed the snakes, evidencing various sources of snake colonization and the first cases ofP. aeruginosacross‐contamination between snakes and owners. These observations led to the conclusion thatP. aeruginosabehaves as an opportunistic species within snakes in captivity and that colonization and dissemination occurs consecutively to processes similar to those identified within the hospital. Antibiotic susceptibility testing showed that most isolates had a wild‐type resistance profile except for one persistent clone isolated from both snakes and preys that harboured multiple antimicrobial resistance genes mediated by an integron carrying theqacH,aadB,aadA2 andcmlA10cassettes, and atetA(C)‐carrying transposon. Biocides or antibiotics used in the zoological garden could have led to the acquisition of this integron.
Understanding the inter‐relationship between improved glycaemic control, hypoglycaemia and weight change within a long‐term economic model
Authors: McEwan P. , Evans M. , Kan H. , Bergenheim K. 
Published: November 2009

Background: Current guidelines for the management of type 2 diabetes advocate the attainment of sustained near normal glycaemia levels. Metformin is widely accepted as the treatment of choice for the initiation of pharmacotherapy; however, secondary failure of oral monotherapy occurs in 60% of patients resulting in the need for multiple pharmacotherapies. Therapy‐related consequences of treatment, such as weight gain and hypoglycaemia impact on the cost‐effectiveness profile of various agents. We therefore sought to ascertain the respective contribution of hypoglycaemia, weight change and improved blood glucose control on second‐line therapy options added to metformin. Methods: This study uses a simulation model designed to evaluate the cost utility of new therapies in a population of patients with type 2 diabetes mellitus. Standard model outputs include incidence of micro‐ and macrovascular complications and diabetes‐specific and all‐cause mortality. Results: The mean discounted quality‐adjusted life year (QALY) predicted by the model was 12.31 years. Reducing Glycosylated haemoglobin (HbA1c) by 1% gave a predicted gain of 0.413 QALYs per patient. A 3‐kg weight loss and 30% reduction in hypoglycaemia frequency produced a combined QALY gain of 0.355, whereas the reverse gave a QALY decrement of 0.356. Conclusions: The results of this analysis quantify the QALY decrement that may result from adverse therapy effects. The beneficial effects of improved glycaemic control on QALYs may be offset by characteristic treatment‐specific adverse effects, such as weight gain and hypoglycaemia frequency.
Increased all‐cause and cardiovascular mortality in monogenic diabetes as a result of mutations in the HNF1A gene
Authors: Steele A. M. , Shields B. M. , Shepherd M. , Ellard S. , Hattersley A. T. , Pearson E. R. 
Published: November 2009

Diabet. Med. 27, 157–161 (2010)AbstractAims  To investigate all‐cause and cardiovascular mortality in subjects with diabetes caused by a mutation in the hepatocyte nuclear factor 1α gene (HNF1A).Methods  We identified 39 British families with HNF1A mutations. Consenting individuals were asked details of age and cause of death of parents and siblings. Copies of death certificates were requested from the family or were obtained via the Offices for National Statistics.Results  Data were collated on 241 control subjects and 153 mutation carriers. Of those who died, 66% of mutation carriers died from a cardiovascular‐related illness compared with 43% of control subjects (P = 0.02). Family members with HNF1A mutations died at a younger age than familial control subjects [all‐cause hazard ratio, adjusting for sex and smoking status: 1.9 (95% confidence interval 1.2, 2.9, P = 0.006; cardiovascular hazard ratio: 2.3, confidence interval 1.3, 4.2, P = 0.006)].Conclusions  We have shown that individuals known to have diabetes caused by a mutation in the HNF1A gene have an increased risk of cardiovascular mortality compared with their unaffected family members. As with other forms of diabetes, consideration should be given to early statin therapy despite a seemingly protective lipid profile.
Lower‐limb risk factors for falls in people with diabetes mellitus
Authors: MacGilchrist C. , Paul L. , Ellis B. M. , Howe T. E. , Kennon B. , Godwin J. 
Published: November 2009

Diabet. Med. 27, 162–168 (2010)AbstractBackground  Older people with diabetes mellitus (DM) may be at high risk of falling because of general risk factors for falls as well as disease‐specific factors.Aims  To determine the prevalence of falls and to investigate lower‐limb factors for falls in older people with DM.Methods  Sixty patients with DM over 55 years of age were recruited. ‘Fallers’ were those who self‐reported at least one fall in the previous year. In addition to diabetes status and demographic information, the following were assessed: neuropathy symptom score (NSS), neuropathy disability score (NDS), foot deformity score (FDS), Tinetti performance‐oriented assessment of mobility (POMA), ankle muscle strength and gait parameters. Data from ‘fallers’ and ‘non‐fallers’ were compared and logistic regression analysis performed to identify variables predictive of falls.Results  Thirty‐five per cent (n = 21) of participants had fallen in the preceding year. Compared with ‘non‐fallers’, there was a greater incidence of peripheral neuropathy among ‘fallers’ (86% of ‘fallers’ and 56% of ‘non‐fallers’), higher vibration perception threshold (P = 0.04), slower gait velocity (P < 0.001), lower muscle strength for dorsiflexion, plantarflexion, inversion and eversion (all P < 0.001) and higher incidence of bony prominences and prominent metatarsal heads (both P < 0.001). There was a strong and significant correlation between dorsiflexion muscle strength and gait velocity. Logistic regression analysis determined that walking velocity, strength of ankle dorsiflexors and NSS accurately predicted 75% of ‘fallers’.Conclusions  Simple clinical measures of gait velocity and ankle muscle strength may be used to identify people with DM at risk of falling, allowing preventative strategies to be implemented.
Effect of targeting normal fasting glucose levels with basal insulin glargine on glycaemic variability and risk of hypoglycaemia: a randomized, controlled study in patients with early Type 2 diabetes
Authors: Hanefeld M. , Koehler C. , Hoffmann C. , Wilhelm K. , Kamke W. , Gerstein H. 
Published: November 2009

Diabet. Med. 27, 175–180 (2010)AbstractAims  The purpose of this sub‐study of the Outcome Reduction with Initial Glargine Intervention (ORIGIN) trial was to determine efficacy and safety of targeting normal fasting plasma glucose (FPG) levels in patients with early Type 2 diabetes treated with insulin glargine in comparison with standard care.Methods  Participants were randomly allocated to insulin or standard care. Insulin was titrated to reach FPG ≤ 5.3 mmol/l. Two years after randomization in a small subset (43 glargine, 32 standard care), continuous glucose measurement (CGMS® System Gold™), including a test meal, was performed. Sixteen volunteers with normal oral glucose tolerance test (OGTT) served as control subjects. Objectives were glycaemic variability, standard deviation (sd), mean amplitude of glucose excursion (MAGE) with postprandial glucose excursion after the test meal, time spent < 3.0 mmol/l interstitial glucose.Results  Participants allocated to insulin and standard care had FPG levels of 5.3 and 6.1 mmol/l (P = 0.019) and glycated haemoglobin (HbA1c) 5.7% and 5.9%, respectively (P < 0.025). Time (min/24 h) spent at low glucose levels was not significantly different between groups (30.6 ± 83.8 min control subjects, 33.7 ± 75.1 min insulin, 10.6 ± 50.6 min standard care). Standard deviation and MAGE were similar for glargine and standard care, but significantly higher than in control subjects. If FPG was < 5.3 mmol/l, the postprandial glucose excursion was in the range seen in control subjects.Conclusions  Treatment to target of FPG < 5.3 mmol/l with insulin glargine was not associated with significantly increased risk of hypoglycaemia. Strict control of FPG with insulin glargine was effective to control postprandial glucose excursion, but had no significant effect on sd and MAGE.
Polymorphisms of the macrophage migration inhibitory factor gene in a UK population with Type 1 diabetes mellitus
Authors: Martin R. J. L. , Savage D. A. , Carson D. J. , McKnight A. J. , Maxwell A. P. , Patterson C. C. 
Published: November 2009

Diabet. Med. 27, 143–149 (2010)AbstractAims  Macrophage migration inhibitory factor (MIF) is a potent pro‐inflammatory cytokine whose production is transcriptionally regulated by glucose. Experimental data from both Type 1 diabetes mellitus (T1D) patients and animal models suggests a role for MIF in the development of T1D. The aim of this study was to employ gene resequencing to identify common DNA polymorphisms in the MIF gene and subsequently assess haplotype tagged single nucleotide polymorphisms (htSNPs) using a combination of case–control and family‐based association analyses in order to assess the association of MIF htSNPs with the development of T1D in a white population.Methods  All exons, introns and approximately 3 kb upstream and downstream of the MIF gene were screened for DNA polymorphisms in 46 individuals using DNA sequencing. Genotyping of the htSNPs was performed in 432 cases, 407 control subjects and 290 T1D parent–offspring trios, using Taqman, Sequenom, Pyrosequencing and fluorescence‐based microsatellite technologies.Results  Twenty‐three polymorphisms (two novel) with a minor allele frequency > 10% were identified. Four MIF htSNPs (rs875643 G>A, rs7388067 C>T, rs5844572 −/CATT, rs6003941 T>G) were identified. Allele and haplotype frequencies were similar between case and control groups (P > 0.6 by permutation test) and assessment of allele transmission distortion from informative parents to affected offspring also failed to find an association. Stratification of these analyses for age‐at‐onset and human leukocyte antigen (HLA)‐DR risk group (DR3/DR4) did not reveal any significant associations.Conclusions  It is unlikely that common polymorphisms in the MIF gene strongly influence susceptibility to T1D in the UK population.
A method of identifying and correcting miscoding, misclassification and misdiagnosis in diabetes: a pilot and validation study of routinely collected data
Authors: De Lusignan S. , Khunti K. , Belsey J. , Hattersley A. , Van Vlymen J. , Gallagher H. , Millett C. , Hague N. J. , Tomson C. , Harris K. , Majeed A. 
Published: November 2009

Diabet. Med. 27, 203–209 (2010)AbstractAims  Incorrect classification, diagnosis and coding of the type of diabetes may have implications for patient management and limit our ability to measure quality. The aim of the study was to measure the accuracy of diabetes diagnostic data and explore the scope for identifying errors.Method  We used two sets of anonymized routinely collected computer data: the pilot used Cutting out Needless Deaths Using Information Technology (CONDUIT) study data (n = 221 958), which we then validated using 100 practices from the Quality Improvement in Chronic Kidney Disease (QICKD) study (n = 760 588). We searched for contradictory diagnostic codes and also compatibility with prescription, demographic and laboratory test data. We classified errors as: misclassified—incorrect type of diabetes; misdiagnosed—where there was no evidence of diabetes; or miscoded—cases where it was difficult to infer the type of diabetes.Results  The standardized prevalence of diabetes was 5.0 and 4.0% in the CONDUIT and the QICKD data, respectively: 13.1% (n = 930) of CONDUIT and 14.8% (n = 4363) QICKD are incorrectly coded; 10.3% (n = 96) in CONDUIT and 26.2% (n = 1143) in QICKD are misclassified; nearly all of these cases are people classified with Type 1 diabetes who should be classified as Type 2. Approximately 5% of T2DM in both samples have no objective evidence to support a diagnosis of diabetes. Miscoding was present in approximately 7.8% of the CONDUIT and 6.1% of QICKD diabetes records.Conclusions  The prevalence of miscoding, misclassification and misdiagnosis of diabetes is high and there is substantial scope for further improvement in diagnosis and data quality. Algorithms which identify likely misdiagnosis, misclassification and miscoding could be used to flag cases for review.
3‐D visualization and animation technologies in anatomical imaging
Authors: McGhee John 
Published: November 2009

AbstractThis paper explores a 3‐D computer artist’s approach to the creation of three‐dimensional computer‐generated imagery (CGI) derived from clinical scan data. Interpretation of scientific imagery, such as magnetic resonance imaging (MRI), is restricted to the eye of the trained medical practitioner in a clinical or scientific context. In the research work described here, MRI data are visualized and interpreted by a 3‐D computer artist using the tools of the digital animator to navigate image complexity and widen interaction. In this process, the artefact moves across disciplines; it is no longer tethered to its diagnostic origins. It becomes an object that has visual attributes such as light, texture and composition, and a visual aesthetic of its own. The introduction of these visual attributes provides a platform for improved accessibility by a lay audience. The paper argues that this more artisan approach to clinical data visualization has a potential real‐world application as a communicative tool for clinicians and patients during consultation.
Anatomical models and wax Venuses: art masterpieces or scientific craft works?
Authors: Ballestriero R. 
Published: November 2009

AbstractThe art of wax modelling has an ancient origin but rose to prominence in 14th century Italy with the cult of votive artefacts. With the advent of Neoclassicism this art, now deemed repulsive, continued to survive in a scientific environment, where it flourished in the study of normal and pathological anatomy, obstetrics, zoology and botany. The achievement of having originated the creation of anatomical models in coloured wax must be ascribed to a joint effort undertaken by the Sicilian wax modeller Gaetano Giulio Zumbo and the French surgeon Guillaume Desnoues in the late 17th century. Interest in anatomical wax models spread throughout Europe during the 18th century, first in Bologna with Ercole Lelli, Giovanni Manzolini and Anna Morandi, and then in Florence with Felice Fontana and Clemente Susini. In England, the art of anatomical ceroplastics was brought to London from Florence by the sculptor Joseph Towne. Throughout the centuries many anatomical artists preferred this material due to the remarkable mimetic likeness obtained, far surpassing any other material. Independent of the material used, whether wood, wax or clay, anatomical models were always considered merely craft works confined to hospitals or faculties of medicine and have survived to this day only because of their scientific interest. Italian and English waxes are stylistically different but the remarkable results obtained by Susini and Towne, and the fact that some contemporary artists are again representing anatomical wax bodies in their works, makes the border that formerly separated art and craft indistinguishable.