Long non-coding RNAs as novel components in the TP53 pathway

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Evaluation of a phenology-dependent response method for estimating leaf area index of rice across cllimate gradients

Accurate estimate of the seasonal leaf area index (LAI) in croplands is required for understanding not only intra- and inter-annual crop development, but also crop management. Lack of consideration in different growth phases in the relationship between LAI and vegetation indices (VI) often results in unsatisfactory estimation in the seasonal course of LAI. In this study, we partitioned the growing season into two phases separated by maximum VI ( VI max ) and applied the general regression model to the data gained from two phases. As an alternative method to capture the influence of seasonal phenological development on the LAI-VI relationship, we developed a consistent development curve method and compared its performance with the general regression approaches. We used the Normalized Difference VI (NDVI) and the Enhanced VI (EVI) from the rice paddy sites in Asia (South Korea and Japan) and Europe (Spain) to examine its applicability across different climate conditions and management cycles. When the general regression method was used, separating the season into two phases resulted in no better estimation than the estimation obtained with the entire season observation due to an abrupt change in seasonal LAI occurring during the transition between the before and after VI max . The consistent development curve method reproduced the seasonal patterns of LAI from both NDVI and EVI across all sites better than the general regression method. Despite less than satisfactory estimation of a local LAI max , the consistent development curve method demonstrates improvement in estimating the seasonal course of LAI. The method can aid in providing accurate seasonal LAI as an input into ecological process-based models

Neutrino Factories: Physics Potential

The physics potential of low-performance and high-performance neutrino factories is briefly reviewed..Comment: Talk presented at NUFACT02, London, 1-6 July, 2002. 8 pages, 5 figure

What skills do primary health care professionals need to provide effective self-management support?: seeking consumer perspectives

Author version made available in accordance with the publisher's policyObjective This research aimed to identify the skills required by primary health care (PHC) professionals to provide effective chronic condition prevention and self -management (CCPSM) support, according to the perceptions of a sample of Australian consumers and carers. Methods Qualitative data was collected and integrated from a focus group, key informant interviews and National Stakeholder meetings and a National Workshop, supported by an extensive literature review. Results With the exception of health professionals specifically trained or currently working in this area, consumers and carers perceive there is a lack of understanding, competence and practice of CCPSM support among PHC professionals. Discussion The PHC workforce appears not to have the full set of skills needed to meet the growing burden of chronic conditions on the health system. Recommendations include education and training that focuses on improved communication skills, knowledge of community support resources, identification of consumers' strengths and current capacities, collaborative care with other health professionals, consumers and carers, and psychosocial skills to understand the impact of chronic conditions from the person’s perspective

Polarizing receptor activation dissociates Fibroblast Growth Factor 2 mediated inhibition of myelination from its neuroprotective potential

Fibroblast growth factor (FGF) signaling contributes to failure of remyelination in multiple sclerosis, but targeting this therapeutically is complicated by its functional pleiotropy. We now identify FGF2 as a factor up-regulated by astrocytes in active inflammatory lesions that disrupts myelination via FGF receptor 2 (FGFR2) mediated activation of Wingless (Wnt) signaling; pharmacological inhibition of Wnt being sufficient to abrogate inhibition of myelination by FGF2 in tissue culture. Using a novel FGFR1-selective agonist (F2 V2) generated by deleting the N-terminal 26 amino acids of FGF2 we demonstrate polarizing signal transduction to favor FGFR1 abrogates FGF mediated inhibition of myelination but retains its ability to induce expression of pro-myelinating and immunomodulatory factors that include Cd93, Lif, Il11, Hbegf, Cxcl1 and Timp1. Our data provide new insights into the mechanistic basis of remyelination failure in MS and identify selective activation of FGFR1 as a novel strategy to induce a neuroprotective signaling environment in multiple sclerosis and other neurological diseases

Fibroblast growth factor signalling in multiple sclerosis: inhibition of myelination and induction of pro-inflammatory environment by FGF9

The failure of remyelination in multiple sclerosis is largely unexplained. Lindner et al. report that glial cells in demyelinating lesions show increased expression of fibroblast growth factor 9 (FGF9). This induces astrocyte-dependent responses that inhibit remyelination and stimulate expression of pro-inflammatory chemokines, supporting a feedback loop that amplifies disease activit

Functionalisation of Ti6Al4V components fabricated using selective laser melting with a bioactive compound

Surface modification of an implant with a biomolecule is used to improve its biocompatibility and to reduce post-implant complications. In this study, a novel approach has been used to functionalise phosphonic acid monolayers with a drug. Ti6Al4V components fabricated using selective laser melting (SLM) were functionalised with Paracetamol (a pharmaceutically relevant biomolecule) using phosphonic acid based self-assembled monolayers (SAMs). The attachment, stability of the monolayers on the SLM fabricated surface and functionalisation of SAMs with Paracetamol were studied using X-ray photoelectron spectroscopy (XPS) and surface wettability measurements. The obtained results confirmed that SAMs were stable on the Ti6Al4V surface for over four weeks and then began to desorb from the surface. The reaction used to functionalise the phosphonic acid monolayers with Paracetamol was noted to be successful. Thus, the proposed method has the potential to immobilise drugs/proteins to SAM coated surfaces and improve their biocompatibility and reduce post-implant complications

Fibroblast growth factor signalling in multiple sclerosis:inhibition of myelination and induction of pro-inflammatory environment by FGF9

Remyelination failure plays an important role in the pathophysiology of multiple sclerosis, but the underlying cellular and molecular mechanisms remain poorly understood. We now report actively demyelinating lesions in patients with multiple sclerosis are associated with increased glial expression of fibroblast growth factor 9 (FGF9), which we demonstrate inhibits myelination and remyelination in vitro. This inhibitory activity is associated with the appearance of multi-branched ‘pre-myelinating’ MBP+/PLP+ oligodendrocytes that interact with axons but fail to assemble myelin sheaths; an oligodendrocyte phenotype described previously in chronically demyelinated multiple sclerosis lesions. This inhibitory activity is not due to a direct effect of FGF9 on cells of the oligodendrocyte lineage but is mediated by factors secreted by astrocytes. Transcriptional profiling and functional validation studies demonstrate that these include effects dependent on increased expression of tissue inhibitor of metalloproteinase-sensitive proteases, enzymes more commonly associated with extracellular matrix remodelling. Further, we found that FGF9 induces expression of Ccl2 and Ccl7, two pro-inflammatory chemokines that contribute to recruitment of microglia and macrophages into multiple sclerosis lesions. These data indicate glial expression of FGF9 can initiate a complex astrocyte-dependent response that contributes to two distinct pathogenic pathways involved in the development of multiple sclerosis lesions. Namely, induction of a pro-inflammatory environment and failure of remyelination; a combination of effects predicted to exacerbate axonal injury and loss in patients