bluuebunny/crossref_metadata_2025_split huggingface dataset:
pH dependency of sclerotial development and pathogenicity revealed by using genetically defined oxalate‐minus mutants of Sclerotinia sclerotiorum
Authors: Xu Liangsheng , Xiang Meichun , White David , Chen Weidong 
Published: February 2015

SummaryThe devastating plant pathogen Sclerotinia sclerotiorum produces copious (up to 50 mM) amounts of oxalic acid, which, for over a quarter century, has been claimed as the pathogenicity determinant based on UV‐induced mutants that concomitantly lost oxalate production and pathogenicity. Such a claim was made without fulfilling the molecular Koch's postulates because the UV mutants are genetically undefined and harbour a developmental defect in sclerotial production. Here, we generated oxalate‐minus mutants of S. sclerotiorum using two independent mutagenesis techniques, and tested the resulting mutants for growth at different pHs and for pathogenicity on four host plants. The oxalate‐minus mutants accumulated fumaric acid, produced functional sclerotia and have reduced ability to acidify the environment. The oxalate‐minus mutants retained pathogenicity on plants, but their virulence varied depending on the pH and buffering capacity of host tissue. Acidifying the host tissue enhanced virulence of the oxalate‐minus mutants, whereas supplementing with oxalate did not. These results suggest that it is low pH, not oxalic acid itself, that establishes the optimum conditions for growth, reproduction, pathogenicity and virulence expression of S. sclerotiorum. Exonerating oxalic acid as the primary pathogenicity determinant will stimulate research into identifying additional candidates as pathogenicity factors towards better understanding and managing Sclerotinia diseases.
Household Asset‐Holding Diversification in Australia
Authors: Mariotti Francesco , Mumford Karen , Pena‐Boquete Yolanda 
Published: February 2015

AbstractWe explore asset‐holding diversification by Australian households; in particular, the household asset diversification participation decision (whether or not to diversify at all) is jointly estimated with the decision of how much to diversify. In so doing, recent literature on the modelling of proportions is combined with the growing body of research concerning household financial decision‐making. Our findings are consistent with the participation of households operating in diverse financial markets being constrained by ineffective information conduits, influencing the decision of whether or not to diversify.
Do altered energy metabolism or spontaneous locomotion ‘mediate’ decelerated senescence?
Authors: Arum Oge , Dawson John Alexander , Smith Daniel Larry , Kopchick John J. , Allison David B. , Bartke Andrzej 
Published: February 2015

SummaryThat one or multiple measures of metabolic rate may be robustly associated with, or possibly even causative of, the progression of aging‐resultant phenotypes such as lifespan is a long‐standing, well‐known mechanistic hypothesis. To broach this hypothesis, we assessed metabolic function and spontaneous locomotion in two genetic and one dietary mouse models for retarded aging, and subjected the data to mediation analyses to determine whether any metabolic or locomotor trait could be identified as a mediator of the effect of any of the interventions on senescence. We do not test the hypothesis of causality (which would require some experiments), but instead test whether the correlation structure of certain variables is consistent with one possible pathway model in which a proposed mediating variable has a causal role. Results for metabolic measures, including oxygen consumption and respiratory quotient, failed to support this hypothesis; similar negative results were obtained for three behavioral motion metrics. Therefore, our mediation analyses did not find support that any of these correlates of decelerated senescence was a substantial mediator of the effect of either of these genetic alterations (with or without caloric restriction) on longevity. Further studies are needed to relate the examined phenotypic characteristics to mechanisms of aging and control of longevity.
Rifampicin reduces advanced glycation end products and activates DAF‐16 to increase lifespan in Caenorhabditis elegans
Authors: Golegaonkar Sandeep , Tabrez Syed S. , Pandit Awadhesh , Sethurathinam Shalini , Jagadeeshaprasad Mashanipalya G. , Bansode Sneha , Sampathkumar Srinivasa‐Gopalan , Kulkarni Mahesh J. , Mukhopadhyay Arnab 
Published: February 2015

SummaryAdvanced glycation end products (AGEs) are formed when glucose reacts nonenzymatically with proteins; these modifications are implicated in aging and pathogenesis of many age‐related diseases including type II diabetes, atherosclerosis, and neurodegenerative disorders. Thus, pharmaceutical interventions that can reduce AGEs may delay age‐onset diseases and extend lifespan. Using LC‐MSE, we show that rifampicin (RIF) reduces glycation of important cellular proteins in vivo and consequently increases lifespan in Caenorhabditis elegans by up to 60%. RIF analog rifamycin SV (RSV) possesses similar properties, while rifaximin (RMN) lacks antiglycation activity and therefore fails to affect lifespan positively. The efficacy of RIF and RSV as potent antiglycating agents may be attributed to the presence of a p‐dihydroxyl moiety that can potentially undergo spontaneous oxidation to yield highly reactive p‐quinone structures, a feature absent in RMN. We also show that supplementing rifampicin late in adulthood is sufficient to increase lifespan. For its effect on longevity, rifampicin requires DAF‐18 (nematode PTEN) as well as JNK‐1 and activates DAF‐16, the FOXO homolog. Interestingly, the drug treatment modulates transcription of a different subset of DAF‐16 target genes, those not controlled by the conserved Insulin‐IGF‐1‐like signaling pathway. RIF failed to increase the lifespan of daf‐16 null mutant despite reducing glycation, showing thereby that DAF‐16 may not directly affect AGE formation. Together, our data suggest that the dual ability to reduce glycation in vivo and activate prolongevity processes through DAF‐16 makes RIF and RSV effective lifespan‐extending interventions.
Long‐lived Snell dwarf mice display increased proteostatic mechanisms that are not dependent on decreased mTORC1 activity
Authors: Drake Joshua C. , Bruns Danielle R. , Peelor Frederick F. , Biela Laurie M. , Miller Richard A. , Miller Benjamin F. , Hamilton Karyn L. 
Published: February 2015

SummaryMaintaining proteostasis is thought to be a key factor in slowed aging. In several growth‐restricted models of long‐life, we have shown evidence of increased proteostatic mechanisms, suggesting that proteostasis may be a shared characteristic of slowed aging. The Snell dwarf mouse is generated through the mutation of the Pit‐1 locus causing reductions in multiple hormonal growth factors and mTORC1 signaling. Snell dwarfs are one of the longest lived rodent models of slowed aging. We hypothesized that proteostatic mechanisms would be increased in Snell compared to control (Con) as in other models of slowed aging. Using D2O, we simultaneously assessed protein synthesis in multiple subcellular fractions along with DNA synthesis in skeletal muscle, heart, and liver over 2 weeks in both sexes. We also assessed mTORC1‐substrate phosphorylation. Skeletal muscle protein synthesis was decreased in all protein fractions of Snell compared to Con, varied by fraction in heart, and was not different between groups in liver. DNA synthesis was lower in Snell skeletal muscle and heart but not in liver when compared to Con. The new protein to new DNA synthesis ratio was increased threefold in Snell skeletal muscle and heart compared to Con. Snell mTORC1‐substrate phosphorylation was decreased only in heart and liver. No effect of sex was seen in this study. Together with our previous investigations in long‐lived models, we provide evidence further supporting proteostasis as a shared characteristic of slowed aging and show that increased proteostatic mechanisms may not necessarily require a decrease in mTORC1.
Effects of heat on the germination of sclerophyllous forest species in the highlands of Madagascar
Authors: Alvarado Swanni T. , Buisson Elise , Rabarison Harison , Rajeriarison Charlotte , Birkinshaw Chris , Lowry Porter P. 
Published: February 2015

AbstractThe effects of fire on germination have been extensively studied in many ecosystems. Several studies have shown that plant species in ecosystems frequently exposed to fire can survive through two main mechanisms: vegetative regeneration (re‐sprouts) and recruitment of new individuals from a fire‐resistant seed bank. In Africa, an increase in temperature can break seed dormancy and stimulate germination of some herbaceous and woody species. In Madagascar, the once widespread highland ecosystems dominated by woody species are now highly fragmented and dominated by anthropic grasslands and fields, with a significantly reduced area occupied by sclerophyllous forests referred to as ‘tapia woodlands’. Six species of this endemic vegetation type were studied: Abrahamia ibityensis (Anacardiaceae), Aphloia theiformis (Aphloiaceae), Carissa edulis (Apocynaceae), Pentachlaena latifolia (Sarcolaenaceae), Uapaca bojeri (Phyllanthaceae) and Vaccinium secundiflorum (Ericaceae). Germination tests were conducted (i) by soaking seeds in water for 24 h (imbibition) or (ii) by exposing the seeds to dry heat. Four different temperatures (40, 60, 80 and 120°C) were applied, and seeds were exposed for 10, 30, 60 and 90 min. To simulate hotter faster‐burning fires, two higher temperatures (100 and 120°C) were also used by exposing seeds to dry heat for 5 min. The results did not reveal any significant effect of 24‐h water imbibition on germination. For most species, germination decreased with increasing temperature of treatment using dry heat. Uapaca bojeri did not germinate under any treatment. Further studies on the biological and ecological characteristics of tapia woodland species in response to fire are needed to help guide conservation, management and restoration activities focusing on this endemic vegetation type.
Offspring performance and recruitment of the pioneer treeAcacia caven(Fabaceae) in a fragmented subtropical dry forest
Authors: Ashworth Lorena , Calviño Ana , Martí María Leticia , Aguilar Ramiro 
Published: February 2015

AbstractThe process of habitat fragmentation results in the breaking apart of originally continuous habitats, causing multiple changes in biotic and abiotic interactions. Alterations in resource availability and in mutualistic and antagonistic plant–animal interactions may impact plant offspring quantity and quality. Currently, several old fragmented systems evidence a process of flora homogenization, where shade‐tolerant species are replaced by pioneer light‐demanding species. Notably, the relationship between quantity and quality parameters of plant offspring production and the successful recruitment of pioneer species in fragmented forests has been poorly explored. Here, we assess population size, sapling recruitment and offspring performance of one of the most widespread tree species of subtropicalSouthAmerica, the native pioneerAcacia caven(Fabaceae). Population size of adults and saplings increased from small to continuous forests, whereas the sapling recruitment per adult tree (sapling/adult ratio) showed no significant differences among forests of different size. Seedling performance was negatively related to forest area and population size, implying potential superior competitive ability of seedlings produced in smaller populations compared to larger ones. Our results show thatA. cavenis resilient to habitat fragmentation effects, which may be ascribed to a set of advantageous ecological traits such as outcrossing, massive flowering, generalist pollination, drought resistance, rapid growth and re‐sprouting. Thus, this pioneer tree benefits from the availability of vacant sites and resources released by declining plant populations of other species, eventually becoming the dominant species in fragmented habitats. Pioneer native plant species with ecological traits such asA. cavenmay represent the silent successful survivors and new colonizers of fragmented habitats, the ubiquitous landscapes of the future.
Does ear keloid formation depend on the type of earrings or piercing jewellery?
Authors: Hochman† Bernardo , Isoldi Felipe C , Silveira Tiago S , Borba Graizela C , Ferreira Lydia M 
Published: February 2015

AbstractThe ear is one of the most common sites of keloid formation, usually associated with the wearing of earrings. However, although this is a small perforating lesion that is equal on both sides, keloids are bigger and more prevalent on the posterior surface. In this study, 141 keloids were evaluated, most of which were located on the posterior surface of the earlobe and caused by the piercing of the ear. Most of the earrings and piercing jewellery used had metallic backs. The more frequent occurrence of earlobe keloids on the posterior surface of the ear therefore may be associated with the exacerbation of local neurogenic inflammation caused by the metallic backs.
Current landscape for treatment of advanced basal cell carcinoma
Authors: Foley Peter 
Published: February 2015

AbstractBasal cell carcinomas (BCCs) account for around 80% of non‐melanoma skin cancer. Australia has the highest incidence of BCC globally and the rates continue to increase in both Australia and New Zealand. BCC causes significant morbidity, placing an enormous burden on the healthcare system. Treatment of patients with advanced BCC can be particularly challenging. A panel of UK experts recently defined advanced disease as BCC that in which current treatment modalities are considered potentially contraindicated by clinical or patient‐driven factors. Research has found that mutations in the hedgehog signalling pathway underpin the pathogenesis of the vast majority of sporadic BCC, as well as Gorlin syndrome. The first‐in‐class oral small molecule hedgehog pathway inhibitor – vismodegib–is now approved in a number of countries for use in locally‐advanced and metastatic BCC and has resulted in improved outcomes in the majority of patients treated. With a number of similar agents in the pipeline, research is now focusing on identifying mechanisms that may contribute to resistance to this agent in some lesions.
Remote ischaemic conditioning: cardiac protection from afar
Authors: Sivaraman V. , Pickard J. M. J. , Hausenloy D. J. 
Published: February 2015

AbstractFor patients with ischaemic heart disease, remote ischaemic conditioning may offer an innovative, non‐invasive and virtually cost‐free therapy for protecting the myocardium against the detrimental effects of acute ischaemia‐reperfusion injury, preserving cardiac function and improving clinical outcomes. The intriguing phenomenon of remote ischaemic conditioning was first discovered over 20 years ago, when it was shown that the heart could be rendered resistant to acute ischaemia‐reperfusion injury by applying one or more cycles of brief ischaemia and reperfusion to an organ or tissue away from the heart – initially termed ‘cardioprotection at a distance’. Subsequent pre‐clinical and then clinical studies made the important discovery that remote ischaemic conditioning could be elicited non‐invasively, by inducing brief ischaemia and reperfusion to the upper or lower limb using a cuff. The actual mechanism underlying remote ischaemic conditioning cardioprotection remains unclear, although a neuro‐hormonal pathway has been implicated. Since its initial discovery in 1993, the first proof‐of‐concept clinical studies of remote ischaemic conditioning followed in 2006, and now multicentre clinical outcome studies are underway. In this review article, we explore the potential mechanisms underlying this academic curiosity, and assess the success of its application in the clinical setting.
Dopamine and T cells: dopamine receptors and potent effects on T cells, dopamine production in T cells, and abnormalities in the dopaminergic system in T cells in autoimmune, neurological and psychiatric diseases
Authors: Levite M. 
Published: February 2015

AbstractDopamine, a principal neurotransmitter, deserves upgrading to ‘NeuroImmunotransmitter’ thanks to its multiple, direct and powerful effects on most/all immune cells. Dopamine by itself is a potent activator of resting effector T cells (Teffs), via two independent ways: direct Teffs activation, and indirect Teffs activation by suppression of regulatory T cells (Tregs). The review covers the following findings: (i) T cells express functional dopamine receptors (DRs) D1R‐D5R, but their level and function are dynamic and context‐sensitive, (ii)DRmembranal protein levels do not necessarily correlate withDR mRNAlevels, (iii) different T cell types/subtypes have differentDRlevels and composition and different responses to dopamine, (iv) autoimmune and pro‐inflammatory T cells and T cell leukaemia/lymphoma also express functionalDRs, (v) dopamine (~10−8M) activates resting/naive Teffs (CD8+>>>CD4+), (vi) dopamine affects Th1/Th2/Th17 differentiation, (vii) dopamine inhibits already activated Teffs (i.e. T cells that have been already activated by either antigen, mitogen, anti‐CD3 antibodies cytokines or other molecules), (viii) dopamine inhibits activated Tregs in an autocrine/paracrine manner. Thus, dopamine ‘suppresses the suppressors’ and releases the inhibition they exert on Teffs, (ix) dopamine affects intracellular signalling molecules and cascades in T cells (e.g.ERK, Lck, Fyn,NF‐κB,KLF2), (x) T cells produce dopamine (Tregs>>>Teffs), can release dopamine, mainly after activation (by antigen, mitogen, anti‐CD3 antibodies, PKC activators or other), uptake extracellular dopamine, and most probably need dopamine, (xi) dopamine is important for antigen‐specific interactions between T cells and dendritic cells, (xii) in few autoimmune diseases (e.g. multiple sclerosis/SLE/rheumatoid arthritis), and neurological/psychiatric diseases (e.g. Parkinson disease, Alzheimer's disease, Schizophrenia and Tourette), patient's T cells seem to have abnormalDRs expression and/or responses to dopamine or production of dopamine, (xiii) drugs that affect the dopaminergic system have potent effects on T cells (e.g. dopamine=Intropin, L‐dopa, bromocriptine, haloperidol, quinpirole, reserpine, pergolide, ecopipam, pimozide, amantadine, tetrabenazine, nomifensine, butaclamol). Dopamine‐induced activation of resting Teffs and suppression of Tregs seem beneficial for health and may also be used for immunotherapy of cancer and infectious diseases. Independently, suppression ofDRs in autoimmune and pro‐inflammatory T cells, and also in cancerous T cells, may be advantageous. The review is relevant to Immunologists, Neurologists, Neuroimmunologists, Hematologists, Psychiatrists, Psychologists and Pharmacologists.
Sampling of the anterior apical region results in increased cancer detection and upgrading in transrectal repeat saturation biopsy of the prostate
Authors: Seles Maximilian , Gutschi Thomas , Mayrhofer Katrin , Fischereder Katja , Ehrlich Georg , Gallé Guenter , Gutschi Stefan , Pachernegg Oliver , Pummer Karl , Augustin Herbert 
Published: February 2015

ObjectiveTo evaluate whether biopsy cores taken via a transrectal approach from the anterior apical region of the prostate in a repeat‐biopsy population can result in an increased overall cancer detection rate and in more accurate assessment of the Gleason score.Patients and MethodsThe study was a prospective, randomised (end‐fire vs side‐fire ultrasound probe) evaluation of 288 men by repeat transrectal saturation biopsy with 28 cores taken from the transition zone, base, mid‐lobar, anterior and the anterior apical region located ventro‐laterally to the urethra of the peripheral zone.ResultsThe overall prostate cancer detection rate was 44.4%. Improvement of the overall detection rate by 7.8% could be achieved with additional biopsies of the anterior apical region. Two tumours featuring a Gleason score 7 could only be detected in the anterior apical region. In three cases (2.34%) Gleason score upgrading was achieved by separate analysis of each positive core of the anterior apical region. A five‐fold higher cancer detection rate in the anterior apical region compared with the transition zone could be shown.ConclusionSampling of the anterior apical region results in higher overall cancer detection rate in repeat transrectal saturation biopsies of the prostate. Specimens from this region can detect clinically significant cancer, improve accuracy of the Gleason Scoring and therefore may alter therapy.
Clonotypically similar hybridαβT cell receptors can exhibit markedly different surface expression, antigen specificity and cross-reactivity
Authors: Motozono C , Bridgeman J S , Price D A , Sewell A K , Ueno T 
Published: February 2015

SummaryEmerging data indicate that particular major histocompatibility complex (MHC)-bound antigenic peptides can be recognized by identical or near-identical αβ T cell receptors (TCRs) in different individuals. To establish the functional relevance of this phenomenon, we artificially paired α and β chains from closely related TCRs specific for the human leucocyte antigen (HLA)-B*35:01-restricted HIV-1 negative regulatory factor (Nef)-derived epitope VY8 (VPLRPMTY, residues 74–81). Several hybrid TCRs generated in this manner failed to express at the cell surface, despite near homology with naturally isolated αβ chain combinations. Moreover, a substantial proportion of those αβ TCRs that did express lost specificity for the index VY8 peptide sequence. One such hybrid αβ pair gained neo-variant specificity in the context of the VY8 backbone. Collectively, these data show that clonotypically similar TCRs can display profound differences in surface expression, antigen specificity and cross-reactivity with potential relevance for the control of mutable viruses.
Influence of Maxillary Sinus Width on Transcrestal Sinus Augmentation Outcomes: Radiographic Evaluation Based on Cone Beam CT
Authors: Zheng Xiaofei , Teng Minhua , Zhou Fengjuan , Ye Jun , Li Guanda , Mo Anchun 
Published: February 2015

AbstractBackgroundMaxillary sinus elevation is a predictable procedure to vertically enhance bone volume in the posterior maxilla for successful implant placement. It is speculated that graft bone resorption and remodeling which require angiogenesis may be affected by the dimensions of maxillary sinus cavity.PurposeThe aim of this study is to investigate the effect of sinus width (SW) on the outcomes of transcrestal sinus lift with simultaneous implant placement based on cone beam CT (CBCT).Materials and MethodsA total of 57 elevated sites in 33 patients were included in this study. All the patients were treated with transcrestal sinus lift procedure associated with simultaneous implant placement using a composite graft material of autogenous bone and Bio‐Oss. For each patient, CBCT scans were performed preoperatively, immediately after surgery and 6 months after surgery. Measurements of the linear parameters were conducted on the preoperative and postoperative CBCT images. The correlation of SW with graft resorption (GR) was analyzed using Pearson's correlation test with or without the classification of residual bone height.ResultsThe average width of maxillary sinus was 13.68 ± 2.66 mm. The mean height of apical graft bone decreased from 2.85 mm immediately after surgery to 1.38 mm after 6 months. A positive association between SW and GR (r = 0.323, p = .014) was found in general.ConclusionThe findings show that graft bone resorption in elevated sinus has a positive correlation with the SW.