bluuebunny/crossref_metadata_2025_split huggingface dataset:
Is diet segregation between dabbling ducks due to food partitioning? A review of seasonal patterns in the Western Palearctic
Authors: Brochet A.‐L. , Dessborn L. , Legagneux P. , Elmberg J. , Gauthier‐Clerc M. , Fritz H. , Guillemain M. 
Published: October 2011

AbstractWithin the paradigm of resource‐limited competition‐structured communities, dabbling ducks (Anas spp.) have been used as a textbook example of how morphological differences, notably bill lamellar density and body length, may allow sympatric species to partition food and hence coexist. We reviewed all accessible diet studies from the Western Palearctic for three closely related dabbling duck species, mallard (Anas platyrhynchos), pintail (A. acuta) and teal (A. crecca), and present a comprehensive list of the food items (invertebrates, seeds, vegetative parts of plants) ingested. To assess the circumannual perspective of niche separation, we evaluated size distribution of ingested seeds among seasons and duck species. There was a significant difference among duck species in mean size and mass of ingested seeds, as well as in diet composition, with the largest seeds consumed by the largest species (mallard) with the coarsest bill filter apparatus (lamellae), and the smallest seeds by the smallest species (teal) with the finest bill lamellae. However, no effect of season was found, suggesting consistent diet segregation among species throughout the annual cycle of ducks and over large geographical areas. We argue that the patterns of food size separation between the three species are compatible with the idea of coexistence under interspecific competition.
Myo‐inositol hexakisphosphate, isolated from female gametophyte tissue of loblolly pine, inhibits growth of early‐stage somatic embryos
Authors: Wu Di , Cameron Sullards M. , Oldham Charlie D. , Gelbaum Les , Lucrezi Jacob , Pullman Gerald S. , May Sheldon W. 
Published: October 2011

Summary
Myo‐inositol hexakisphosphate (InsP6), abundant in animals and plants, is well known for its anticancer activity. However, many aspects of InsP6 function in plants remain undefined. We now report the first evidence that InsP6 can inhibit cellular proliferation in plants under growth conditions where phosphorus is not limited.
A highly anionic molecule inhibitory to early‐stage somatic embryo growth of loblolly pine (LP) was purified chromatographically from late‐stage LP female gametophytes (FGs), and then characterized structurally using mass spectrometry (MS) and nuclear magnetic resonance (NMR) analyses.
Exact mass and mass spectrometry‐mass spectrometry (MS‐MS) fragmentation identified the bioactive molecule as an inositol hexakisphosphate. It was then identified as the myo‐isomer (i.e. InsP6) on the basis of 1H‐, 31P‐ and 13C‐NMR, 1H‐1H correlation spectroscopy (COSY), 1H‐31P heteronuclear single quantum correlation (HSQC) and 1H‐13C HSQC. Topical application of InsP6 to early‐stage somatic embryos indeed inhibits embryonic growth.
Recently evidence has begun to emerge that InsP6 may also play a regulatory role in plant cells. We anticipate that our findings will help to stimulate additional investigations aimed at elucidating the roles of inositol phosphates in cellular growth and development in plants.
Understanding niche shifts: using current and historical data to model the invasive redlegged earth mite, Halotydeus destructor
Authors: Hill Matthew P. , Hoffmann Ary A. , Macfadyen Sarina , Umina Paul A. , Elith Jane 
Published: October 2011

AbstractAim  Niche conservatism is key to understanding species responses to environmental stress such as climate change or arriving in new geographical space such as biological invasion. Halotydeus destructor is an important agricultural pest in Australia and has been the focus of extensive surveys that suggest this species has undergone a niche shift to expand its invasive range inland to hotter and drier environments. We employ modern correlative modelling methods to examine niche conservatism in H. destructor and highlight ecological differences between historical and current distributions.Location  Australia and South Africa.Methods  We compile comprehensive distribution data sets for H. destructor, representing the native range in South Africa, its invasive range in Australia in the 1960s (40 yr post‐introduction) and its current range in Australia. Using MAXENT, we build correlative models and reciprocally project them between South Africa and Australia and investigate range expansion with models constructed for historical and current data sets. We use several recently developed model exploration tools to examine the climate similarity between native and invasive ranges and subsequently examine climatic variables that limit distributions.Results  The invasive niche of H. destructor in Australia transgresses the native niche in South Africa, and the species has expanded in Australia beyond what is predicted from the native distribution. Our models support the notion that H. destructor has undergone a more recent range shift into hotter and drier inland areas of Australia since establishing a stable distribution in the 1960s.Main conclusions  Our use of historical and current data highlights that invasion is an ongoing dynamic process and demonstrates that once a species has reached an established range, it may still expand at a later stage. We also show that model exploration tools help understand factors influencing the range of invasive species. The models generate hypotheses about adaptive shifts in H. destructor.
Biased signalling and allosteric machines: new vistas and challenges for drug discovery
Authors: Kenakin Terry P 
Published: October 2011

Seven transmembrane receptors (7TMRs) are nature's prototype allosteric proteins made to bind molecules at one location to subsequently change their shape to affect the binding of another molecule at another location. This paper attempts to describe the divergent 7TMR behaviours (i.e. third party allostery, receptor oligomerization, biased agonism) observed in pharmacology in terms of a homogeneous group of allosteric behaviours. By considering the bodies involved as a vector defined by a modulator, conduit and guest, these activities can all be described by a simple model of functional allostery made up of the Ehlert allosteric model and the Black/Leff operational model. It will be shown how this model yields parameters that can be used to characterize the activity of any ligand or protein producing effect through allosteric interaction with a 7TMR.LINKED ARTICLES This article is part of a themed section on the Molecular Pharmacology of G Protein‐Coupled Receptors (GPCRs). To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2012.165.issue‐6. To view the 2010 themed section on the same topic visit http://onlinelibrary.wiley.com/doi/10.1111/bph.2010.159.issue‐5/issuetoc
Reason for clozapine cessation
Authors: Pai N. B. , Vella S. C. 
Published: October 2011

Pai NB, Vella SC. Reason for clozapine cessation.Objective:  Approximately 30% of individuals diagnosed with schizophrenia suffer from treatment‐resistant or refractory schizophrenia. The gold standard for treatment of refractory schizophrenia is clozapine. However, a significant number of patients cease clozapine therapy; therefore this study explores patient’s motives for cessation.Method:  The motives for cessation and duration of clozapine treatment from a retrospective database of 151 patients with schizophrenia or schizo‐affective disorder who had ceased clozapine once or more were reviewed, with the motives for cessation coded. The general motives for cessation were non‐compliance, own decision, medical, poor response and other. In addition, the medical reasons for cessation were further codified: cardiac complications, neutropenia, fevers, other side effects and pregnancy.Results:  The majority of patients ceased clozapine owing to non‐compliance with medical protocols or citing their own decision. Approximately half ceased after a period of 6 months or less. Seventeen per cent of patients ceased owing to medical reasons, with the largest proportions discontinuing treatment because of other side effects or neutropenia.Conclusion:  Future research should seek to further investigate why patients decide to be non‐compliant and formulate their own decision to cease treatment, as this will facilitate strategies to promote adherence amongst these two groups that are potentially the most amenable to change.
Family history and oral health: findings from the Dunedin Study
Authors: Shearer Dara M. , Thomson W. Murray , Caspi Avshalom , Moffitt Terrie E. , Broadbent Jonathan M. , Poulton Richie 
Published: October 2011

Shearer DM, Thomson WM, Caspi A, Moffitt TE, Broadbent JM, Poulton R. Family history and oral health: findings from the Dunedin Family History Study. Community Dent Oral Epidemiol 2011. © 2011 John Wiley & Sons A/SAbstract – Context: The effects of the oral health status of one generation on that of the next within families are unclear.Objectives: To determine whether parental oral health history is a risk factor for oral disease.Methods: Oral examination and interview data were collected during the age‐32 assessments in the Dunedin Study. Parental data were also collected on this occasion. The sample was divided into two familial‐risk groups for caries/tooth loss (high risk and low risk) based on parents’ self‐reported history of tooth loss at the age‐32 assessment interview.Main outcome measures: Probands’ dental caries and tooth loss status at age 32, together with lifelong dental caries trajectory (age 5–32).Results: Caries/tooth loss risk analysis was conducted for 640 proband‐parent groups. Reference groups were the low‐familial‐risk groups. After controlling for confounding factors (sex, episodic use of dental services, socio‐economic status and plaque trajectory), the prevalence ratio (PR) for having lost 1+ teeth by age 32 for the high‐familial‐risk group was 1.41 [95% confidence interval (CI) 1.05, 1.88] and the rate ratio for DMFS at age 32 was 1.41 (95% CI 1.24, 1.60). In the high‐familial‐risk group, the PR of following a high caries trajectory was 2.05 (95% CI 1.37, 3.06). Associations were strongest when information was available about both parents’ oral health. Nonetheless, when information was available for one parent only, associations were significant for some outcomes.Conclusions: People with poor oral health tend to have parents with poor oral health. Family/parental history of oral health is a valid representation of the intricacies of the shared genetic and environmental factors that contribute to an individual’s oral health status. Associations are strongest when data from both parents can be obtained.
Reassessment at 6–7 years of age of a randomized controlled trial initiated before birth to prevent early childhood caries
Authors: Plutzer Kamila , John Spencer A. , Keirse Marc J. N. C. 
Published: October 2011

Plutzer K, Spencer AJ, Keirse MJNC. Reassessment at 6–7 years of age of a randomized controlled trial initiated before birth to prevent early childhood caries. Community Dent Oral Epidemiol 2012; 40: 116–124. © 2011 John Wiley & Sons A/SAbstract –  Objectives:  To assess whether the effect of providing mothers with guidance during pregnancy and when the child was 6 and 12 months old, which had drastically reduced the prevalence of early childhood caries at 20 months of age, would be sustained at 6–7 years of age.Methods:  Children, whose mothers had been enrolled in a randomized controlled trial during pregnancy and a comparison group of similar school children, were examined for the presence of caries by the South Australian School Dental Services (SA SDS) at 6–7 years of age.Results:  Of 625 eligible trial participants, 277 (44%) participated in the follow‐up and dental records were available for 187 of them (30%). Loss to follow‐up and reasons for it were similar in the intervention and control groups. At 6–7 years of age, 33% of children in the trial had caries compared with 42% in the SA SDS comparison group (n = 263). All measures of caries severity (d3mft, d3mfs and SiC30) were lower, but not significantly so, in the intervention than in the control group. Children in the comparison group of school children had more severe caries than those in the trial (P < 0.01) and in the intervention group especially (P < 0.005). Children in both randomized groups suffered significantly less toothache than those in the comparison group (P < 0.001).Conclusions:  Providing new mothers with guidance on caries prevention helps to reduce early childhood caries and has a sustainable effect up to school age.
Caries in adolescence – influence from early childhood
Authors: Alm A. , Wendt L. K. , Koch G. , Birkhed D. , Nilsson M. 
Published: October 2011

Alm A, Wendt LK, Koch G, Birkhed D, Nilsson M. Caries in adolescence – influence from early childhood. Community Dent Oral Epidemiol 2012; 40: 125–133. © 2011 John Wiley & Sons A/SAbstract –  Objective:  To analyse the relationship between caries determinants in early childhood and caries prevalence in proximal surfaces in adolescents at the age of 15 years.Methods:  The present longitudinal study is part of a series of surveys of oral health in 671 children followed from 1 to 15 years of age. Data were selected from examinations, interviews and questionnaires at 1, 3 and 6 years and bitewing radiographs at 15 years of age. Uni‐ and multivariable logistic regression analyses were performed to identify caries‐related determinants. The outcome variable was carious lesions and fillings (DFa) in approximal tooth surfaces at 15 years of age. Statistical comparisons were made between caries‐free teenagers, DFa = 0 and teenagers with DFa > 0, DFa ≥ 4 and DFa ≥ 8, respectively.Results:  In the final logistic regression analyses, caries experience at 6 years and mother’s self‐estimation of her oral health care as being less good to poor remained statistically significant and were related to caries in all three caries groups (i.e. DF > 0, ≥4 and ≥8) at 15 years of age. The consumption of sweets at 1 year remained statistically significant, with a caries experience of DF ≥ 4 and ≥ 8. The variables ‘parents born abroad’ and female gender were statistically significantly associated with DFa ≥ 4 and DFa ≥ 8, respectively. Furthermore, infrequent toothbrushing habits at 3 years of age and failure to attend the examination at 1 year were statistically significantly associated with caries at 15 years in the univariable analyses.Conclusion:  Early caries experience, consumption of sweets at an early age and mother’s self‐estimation of her oral health care as being less good to poor are associated with approximal caries in adolescents. The study indicates that caries determinants identified during early childhood have a strong impact on approximal caries in adolescence.
A European Core Curriculum in Cariology: the knowledge base
Authors: Anderson P. , Beeley J. , Monteiro P. Manarte , de Soet H. , Andrian S. , Amaechi B. , Huysmans M.‐C. D. N. J. M. 
Published: October 2011

AbstractThis paper is part of a series of papers towards a European Core Curriculum in Cariology for undergraduate dental students. The European Core Curriculum in Cariology is the outcome of a joint workshop of the European Organization for Caries Research (ORCA) together with the Association for Dental Education in Europe (ADEE), which was held in Berlin from 27 to 30 June 2010. This paper presents a closer look at the knowledge base as presented in the European Core Curriculum in Cariology. It comprises not only traditional basic sciences, such as anatomy and histology, but also emerging sciences such as molecular biology and nanotechnology and also fields such as behavioural sciences and research methodology. The different supporting competences are elaborated and explained. The problems of implementing a curriculum that truly integrates this foundation knowledge into the clinical teaching are discussed.
Decision‐making and preventive non‐surgical therapy in the context of a European Core Curriculum in Cariology
Authors: Bottenberg P. , Ricketts D. N. J. , Van Loveren C. , Rahiotis C. , Schulte A. G. 
Published: October 2011

AbstractThis paper is part of a series of papers towards a European Core Curriculum in Cariology for undergraduate dental students. The European Core Curriculum in Cariology is the outcome of a joint workshop of the European Organisation for Caries Research (ORCA) together with the Association for Dental Education in Europe (ADEE), which was held in Berlin from 27 to 30 June 2010. The present paper covers decision‐making and non‐surgical treatment. In particular, it will provide some background information on this part of the European core curriculum. The dentist, on graduation, must be competent at applying the principles of prevention of dental hard tissue disease processes (primary prevention) and progression when it has manifested itself (secondary prevention). The competences should apply in differing ways to patients of all ages. Goals of prevention should be clearly defined in order for outcomes to be evaluated, and a dentist should be competent at determining these outcomes. Although this concept is recognised by many academics and experts, clinical teaching, practice and health insurance coverage frequently emphasise surgical treatment. There are many reasons and obstacles that might account for this, and this paper suggests some reasons why this might be and makes suggestions for how these can be addressed in the future. One factor that is essential in the provision of a preventive, non‐surgical approach is that of communication with the patient. However, this unfortunately takes less space in the dental curricula compared with technical skills aimed at restorative procedures; this weighting needs to be more equally balanced.
Degree of mucositis and duration of neutropenia are the major risk factors for early post‐transplant febrile neutropenia and severe bacterial infections after reduced‐intensity conditioning
Authors: Facchini Luca , Martino Rodrigo , Ferrari Angela , Piñana José L. , Valcárcel David , Barba Pere , Granell Miguel , Delgado Julio , Briones Javier , Sureda Anna , Brunet Salut , Sierra Jorge 
Published: October 2011

AbstractBackground and objectives: Whether the intensity of the conditioning regimen affects febrile neutropenia (FN) and severe bacterial infections (SBIs) is not well established. We analyzed the risk factors (RFs) for the development of FN and SBI in the first 100 d post‐transplant in 195 consecutive adult recipients of a reduced‐intensity conditioning allogeneic hematopoietic stem cell transplantation (RIC‐allo). Materials and methods: The RIC regimens consisted of fludarabine plus melphalan (62%) or busulphan (38%) (FluMel or FluBu). SBIs include pneumonia, urinary tract infections, and bacteremia. Results: FN occurred in 141 patients (72%), always in the first 30 d post‐allo‐RIC. However, a SBI occurred in only 27 patients (14%) during this early post‐transplant period (<day +30), while 29 evaluable patients (15%) developed a SBI in the intermediate post‐transplant period (days +31 to +100). In multivariate analysis, RFs for the development of FN included onset of neutropenia before day +5 after allo‐RIC (P < 0.02) and NCI CTC grade III–IV mucosal damage in the first 10 d post‐transplantation (P = 0.03). RFs identified to SBI by multivariate analysis included corticosteroid therapy before day +100 (P < 0.01), mycophenolate mofetil‐based graft‐versus‐host disease (GVHD) prophylaxis (P < 0.01), and previous SBI before day +30 (P < 0.01). The rate of SBI from day +30 to +100 varied according to the number of RFs; thus, the rate of SBI was 1% in patients without any RF, 17% in patients with one RF, 29% with one RFs, and 53% in those with all three RFs. Conclusions: After an RIC‐allo, FN and early SBI occurred mostly in patients with severe mucositis and early‐onset neutropenia, while postengraftment high‐dose steroid therapy for acute GVHD was the major RF.
The cellular and molecular mechanisms for neutropenia in Barth syndrome
Authors: Makaryan Vahagn , Kulik Willem , Vaz Frederic M. , Allen Christopher , Dror Yigal , Dale David C. , Aprikyan Andrew A. 
Published: October 2011

AbstractBarth syndrome (BTHS), a rare, X‐linked, recessive disease, is characterized by neutropenia and cardiomyopathy. BTHS is caused by loss‐of‐function mutations of the tafazzin (TAZ) gene. We developed a model of BTHS by transfecting human HL60 myeloid progenitor cells with TAZ‐specific shRNAs. Results demonstrate a significant downregulation in TAZ expression, mimicking the effects of naturally occurring truncation mutations in TAZ. Flow cytometry analyses of cells with TAZ‐specific, but not scrambled, shRNAs demonstrate nearly twofold increase in the proportion of annexin V‐positive cells and significantly increased dissipation of mitochondrial membrane potential as determined by DIOC6 staining. Transfection of TAZ‐specific shRNA had similar effects in U937 myeloid cells but not in lymphoid cell lines. Further studies in HL60 myeloid progenitor cells revealed aberrant release of cytochrome c from mitochondria and significantly elevated levels of activated caspase‐3 in response to TAZ knockdown. Treatment with caspase‐specific inhibitor zVAD‐fmk resulted in substantially reduced apoptosis to near‐normal levels. These data suggest that neutropenia in BTHS is attributable to increased dissipation of mitochondrial membrane potential, aberrant release of cytochrome c, activation of caspase‐3, and accelerated apoptosis of myeloid progenitor cells, and that this defect can be partially restored in vitro by treatment with caspase‐specific inhibitors.
Therapy‐related acute promyelocytic leukemia: observations relating to APL pathogenesis and therapy*
Authors: Elliott Michelle A. , Letendre Louis , Tefferi Ayalew , Hogan William J. , Hook Christopher , Kaufmann Scott H. , Pruthi Rajiv K. , Pardanani Animesh , Begna Kebede H. , Ashrani Aneel A. , Wolanskyj Alexandra P. , Al‐Kali Aref , Litzow Mark R. 
Published: October 2011

AbstractTherapy‐related acute promyelocytic leukemia (t‐APL) is a well‐recognized form of APL for which the underlying etiology has been well characterized. The pathogenesis of de novo (dn‐APL) remains unknown; but epidemiologic studies have consistently identified increased body mass index (BMI), younger age, and ethnicity as possible risk factors. We analyzed demographics, clinical features, and treatment responses in a contemporary series of 64 patients treated with all‐trans‐retinoic acid and anthracycline‐based therapy to assess for differences in these two etiologically distinct patient groups. Compared with patients with t‐APL (n = 11), those with dn‐APL (n = 53) had a greater median BMI (31.33 vs. 28.48), incidence of obesity (60.4% vs. 27.3%) (P = 0.04), and history of hyperlipidemia (45.3% vs. 18.2%) (P = 0.01). Fewer t‐APL than dn‐APL patients achieved complete remission at 63.6% vs. 92.5% respectively (P = 0.008). This was the result of a higher induction mortality rate of 36.4% vs. 7.5% respectively (P = 0.008). No cases of leukemic resistance were seen in either group. Overall survival (OS) was inferior in t‐APL compared with dn‐APL at 51% vs. 84%, respectively (P < 0.005), primarily as a result of higher induction mortality. Relapse occurred in nine patients (16.1%) overall, but no relapses occurred in the t‐APL cohort. Our observations provide further support for the hypothesis that abnormalities in lipid homeostasis may in some way be of pathogenic importance in dn‐APL. Therapy‐related APL is sensitive to standard therapy with no cases of resistance or relapse seen. The inferior OS of the t‐APL was due to induction mortality, possibly reflecting prior therapy.