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Plants respond to environmental stresses through controlled stem cell maintenance and meristem activity. One level of gene regulation is RNA alternative splicing. However, the mechanistic link between stress, meristem function and RNA splicing is poorly understood. The MERISTEM-DEFECTIVE (MDF) Arabidopsis gene encodes an SR-related family protein, required for meristem function and leaf vascularization, and is the likely orthologue of the human SART1 and yeast Snu66 splicing factors. MDF is required for the correct splicing and expression of key transcripts associated with root meristem function. We identified RSZ33 and ACC1, both known to regulate cell patterning, as splicing targets required for MDF function in the meristem. MDF expression is modulated by osmotic and cold stress, associated with differential splicing and specific isoform accumulation and shuttling between nucleus and cytosol, and acts in part via a splicing target SR34. We propose a model in which MDF controls splicing in the root meristem to promote stemness and to repress stress response, cell differentiation and cell death pathways.

Plants respond to environmental stresses through controlled stem cell maintenance and meristem activity. One level of transcriptional control is RNA alternative splicing. However the mechanistic link between stress, meristem function and RNA splicing is poorly understood. TheMERISTEM-DEFECTIVE(MDF)/DEFECTIVELY ORGANIZED TRIBUTARIES(DOT2) gene of Arabidopsis encodes a SR-related family protein, required for meristem function and leaf vascularization, and is the likely orthologue of the human SART1 and yeast snu66 splicing factors. MDF is required for the correct splicing and expression of key transcripts associated with root meristem function. We identifiedRSZ33andACC1, both known to regulate cell patterning, as splicing targets required for MDF function in the meristem.MDFexpression is modulated by osmotic and cold stress, associated with differential splicing and specific isoform accumulation and shuttling between nucleus and cytosol, and acts in part via a splicing targetSR34. We propose a model in which MDF controls splicing in the root meristem to promote stemness and repress stress response and cell differentiation pathways.Summary statementThe protein MERISTEM-DEFECTIVE regulates Arabidopsis meristem function through its role as a splicing factor, mediated through splicing targets RSZ33, ACC1 and SR34.

Purpose: Autoimmune polyendocrine syndrome type I (APS-1) is a devastating autoimmune disease characterised by mutations in the AIRE gene. Because of failure of negative selection, these patients produce autoreactive B and T cells against affected tissues, which lead to a range of autoimmune manifestations. The rarity of APS-1 and inaccessibility of thymic tissue have limited immunological studies. We here hypothesized that lack of AIRE expression in thymus affect immune cells in blood. Methods: Whole blood microarray analysis (N=16 APS-I patients vs 16 controls) and qPCR of molecules in affected pathways. Single cell sequencing of naïve B cells and flow cytometry analysis of a B cell panel in PBMCs to investigate properties of B cells in APS-I patients compared to age and sex matched healthy controls. Results: We here show significant downregulation of B cell and IFN-I responses in APS-I patients compared to healthy donors in microarray and system biology deconvolution experiments. Single B cell transcriptomics support downregulation of several of the same molecules including CD74, CD40 and CD79A. Flow cytometry protein experiments revealed an imbalance of plasma (higher) vs transitional B cells (lower) in APS-I patients, followed up by a lower level of CD79b within transitional B cells in patients, but a non-consistent higher level of CD74 within this subset. Conclusion: We found disturbances in blood immune cell subsets from APS-I patients. Harmonious lower blood cell levels of the B-cell associated CD79A/B were found compared to healthy controls, but further studies are needed to verify the consistency of our findings.

Mutations in USH2A gene are responsible for the greatest proportion of hearing and vision loss among individuals with Usher Syndrome (USH) and for autosomal recessive non-syndromic retinitis pigmentosa. Mutations on USH2A exon 13 account for more than 35% of the disease causing USH2A variants including the most prevalence point mutation, c.2299delG, a frameshift mutation. The lack of a clinically relevant animal model has been a bottleneck for the development of therapeutics for USH2A related vision loss. Using CRSPR/Cas9 technology, this study establishes a rabbit line carrying an USH2A frameshift mutation on exon12 (equivalent to human USH2A Exon 13) as a novel mammalian animal model of USH2A. The bi-allelic mutant rabbits exhibit hyper reflective signals in FAF indicating RPE damage and OCT changes indicating photoreceptor degeneration as early as 4 months of age. ERG signals of both rod and cone function were reduced in the USH2A mutant rabbits starting from 7 months old and further decreased at 15-22 months old, indicating progressive retinal photoreceptor degeneration, which is further confirmed by retinal histopathology examination. ABR examination showed moderate to server hearing loss in the USH2A mutant rabbits. These results indicated that disruption of USH2A gene in rabbits is sufficient to induce hearing loss and progressive photoreceptor degeneration. To our knowledge, this is the first mammalian animal model of USH2 which closely recapitulates the phenotype of retinitis pigmentosa in human patients. This study supports the use of rabbits as a clinically relevant animal model to understand the pathogenesis and to develop novel therapeutics for Usher Syndrome.

Launched on 2021 December 9, the Imaging X-ray Polarimetry Explorer (IXPE) is a NASA Small Explorer Mission in collaboration with the Italian Space Agency (ASI). The mission will open a new window of investigation—imaging x-ray polarimetry. The observatory features three identical telescopes, each consisting of a mirror module assembly with a polarization-sensitive imaging x-ray detector at the focus. A coilable boom, deployed on orbit, provides the necessary 4-m focal length. The observatory utilizes a three-axis-stabilized spacecraft, which provides services such as power, attitude determination and control, commanding, and telemetry to the ground. During its 2-year baseline mission, IXPE will conduct precise polarimetry for samples of multiple categories of x-ray sources, with follow-on observations of selected targets.

Scheduled to launch in late 2021 the Imaging X-ray Polarimetry Explorer (IXPE) is a Small Explorer Mission designed to open up a new window of investigation -- X-ray polarimetry. The IXPE observatory features 3 identical telescope each consisting of a mirror module assembly with a polarization-sensitive imaging x-ray detector at its focus. An extending beam, deployed on orbit provides the necessary 4 m focal length. The payload sits atop a 3-axis stabilized spacecraft which among other things provides power, attitude determination and control, commanding, and telemetry to the ground. During its 2-year baseline mission, IXPE will conduct precise polarimetry for samples of multiple categories of x-ray sources, with follow-on observations of selected targets. IXPE is a partnership between NASA and the Italian Space Agency (ASI).

Cellular senescence is characterized by an irreversible cell cycle arrest as well as a pro-inflammatory phenotype, thought to contribute to aging and age-related diseases. Neutrophils have essential roles in inflammatory responses; however, in certain contexts their abundance is associated with a number of age-related diseases, including liver disease. The relationship between neutrophils and cellular senescence is not well understood. Here, we show that telomeres in non-immune cells are highly susceptible to oxidative damage caused by neighboring neutrophils. Neutrophils cause telomere dysfunction both in vitro and ex vivo in a ROS-dependent manner. In a mouse model of acute liver injury, depletion of neutrophils reduces telomere dysfunction and senescence. Finally, we show that senescent cells mediate the recruitment of neutrophils to the aged liver and propose that this may be a mechanism by which senescence spreads to surrounding cells. Our results suggest that interventions that counteract neutrophil-induced senescence may be beneficial during aging and age-related disease. publishedVersion

Background No reliable biomarkers exist to guide glucocorticoid (GC) replacement treatment in autoimmune Addison’s disease (AAD), leading to overtreatment with alarming and persistent side effects or undertreatment, which could be fatal. Objective To explore changes in gene expression following different GC replacement doses as a means of identifying candidate transcriptional biomarkers to guide GC replacement in AAD. Methods Step 1: Global microarray expression analysis on RNA from whole blood before and after intravenous infusion of 100 mg hydrocortisone (HC) in 10 patients with AAD. In 3 of the most highly upregulated genes, we performed real-time PCR (rt-PCR) to compare gene expression levels before and 3, 4, and 6 hours after the HC infusion. Step 2: Rt-PCR to compare expression levels of 93 GC-regulated genes in normal versus very low morning cortisol levels in 27 patients with AAD. Results Step 1: Two hours after infusion of 100 mg HC, there was a marked increase in FKBP5, MMP9, and DSIPI expression levels. MMP9 and DSIPI expression levels correlated with serum cortisol. Step 2: Expression levels of CEBPB, DDIT4, FKBP5, DSIPI, and VDR were increased and levels of ADARB1, ARIDB5, and POU2F1 decreased in normal versus very low morning cortisol. Normal serum cortisol levels positively correlated with DSIPI, DDIT4, and FKBP5 expression. Conclusions We introduce gene expression as a novel approach to guide GC replacement in AAD. We suggest that gene expression of DSIPI, DDIT4, and FKBP5 are particularly promising candidate biomarkers of GC replacement, followed by MMP9, CEBPB, VDR, ADARB1, ARID5B, and POU2F1.

SUMMARYTerminal selectors are transcription factors that control the morphological, physiological and molecular features that characterize distinct cell types. Here we use expression analyses and a transgenic reporter line to show thatNvPOU4is expressed in post-mitotic cells that give rise to a diverse set of neural cell types in the sea anemoneNematostella vectensis. We generated a loss-of-function allele by CRISPR/Cas9 and used additional transgenic reporter lines to show that the initial specification of neural cells is not affected in theNvPOU4mutants. Analyses of transcriptomes derived from the mutants and from different neural cell populations revealed thatNvPOU4is required for the execution of the terminal differentiation program of these neural cells. These findings suggest that POU4 genes have ancient functions as terminal selectors for morphologically and functionally highly disparate types of neurons and they provide experimental support for the relevance of terminal selectors for understanding the evolution of cell types.

Mucopolysaccharidoses are a group of rare lysosomal storage diseases caused by a deficiency of enzymes, which breakdown glycosaminoglycans, with consequent dysfunction of affected tissues. Mandibular coronoid hyperplasia, with associated trismus, has been recently described as a feature of the craniofacial abnormalities seen in these patients. However, the details of the surgical and post-operative management of these patients have not been previously documented. This case describes the successful management of severe trismus from coronoid process hyperplasia in a 14-year-old male, utilising an extra-oral approach for bilateral coronoidectomies and removal of exophytic zygomatic bone, followed by immediate and long-term physiotherapy. An improvement of mandibular opening from 8 to 45 mm has been maintained at 18 months post operation.

Objective: Deciding the optimal doses of glucocorticoid (GC) replacement treatment in autoimmune Addison’s disease (AAD) is impeded by the lack of reliable biomarkers. This frequently results in over-treatment, with alarming and persistent side-effects, or under-replacement, which could be fatal. There is a need to think new in the quest for robust biomarkers to optimize GC replacement in AAD at an individual level. Aim: We aimed to identify genes that are consistently up- or down-regulated in patients with AAD in response to different GC replacement doses. This information can be used to establish novel biomarkers to guide GC treatment in AAD. Methods: Step 1: Global microarray expression analysis on RNA from whole blood before and after intravenous infusion of 100 mg hydrocortisone (HC) in 10 patients with AAD. To verify the results, we performed real-time PCR to compare gene expression levels of three of the highly differentially expressed genes (FKBP5, MMP9, and DSIPI) to compare gene expression levels before and two, four, and six hours after the HC infusion. Step 2: Rt-PCR to compare expression levels of 93 GC-regulated genes in normal versus very low morning cortisol levels in 27 patients with AAD. Results: Step 1: Two hours after infusion of 100 mg HC, there was a marked increase in FKBP5, MMP9, and DSIPI expression levels. MMP9 and DSIPI expression levels correlated with serum cortisol. Step 2: Expression levels of CEBPB, DDIT4, FKBP5, DSIPI, and VDR were increased and ADARB1, ARIDB5, and POU2F1 decreased in normal versus very low morning cortisol. Normal serum cortisol levels positively correlated with DSIPI, DDIT4, and FKBP5 expression. Conclusions: We introduce gene expression as a novel approach to guide GC replacement in AAD. We suggest that gene expression of DSIPI, DDIT4, and FKBP5 are particularly promising candidate biomarkers of GC replacement, followed by MMP9, CEBPB, VDR, ADARB1, ARID5B, and POU2F1.

Several states currently have enacted laws that allow for civil commitment for individuals diagnosed with severe substance use disorders. Civil commitment or involuntary commitment refers to the legal process by which individuals with mental illness are court-ordered into inpatient and/or outpatient treatment programs. Although initially civil commitment laws were intended for individuals with severe mental illness, these statutes have been extended to cover individuals with severe substance use disorders. Much of the recent legislation allowing for civil commitment of individuals with substance use disorders has come about in response to the heroin epidemic and is designed to provide an alternative to the unrelenting progression of opioid use disorders. Civil commitment also provides an opportunity for individuals with opioid use disorders to make informed decisions regarding ongoing or continued treatment. However, civil commitment also raises concerns regarding the potential violation of 14th Amendment rights, specifically pertaining to abuses of deprivation of liberty or freedom, which are guaranteed under the 14th Amendment to the United States Constitution. This commentary examines these issues while supporting the need for effective brief civil commitment legislation in all states.

A field study showed that transgenic grapevine rootstocks can provide trans-graft-mediated protection to a wild type scion against Pierce’s disease (PD) development. We individually field-tested two distinct strategies. The first expressed a chimeric antimicrobial protein (CAP) that targeted the functionality of the lipopolysaccharide (LPS) surface of Xylella fastidiosa (Xf), the causative agent of PD. The second expressed a plant polygalacturonase inhibitory protein (PGIP) that prevents PD by inhibiting breakdown of pectin present in primary cell walls. Both proteins are secreted to the apoplast and then into the xylem, where they migrate past the graft union, transiting into the xylem of the grafted scion. Transgenic Vitis vinifera cv. Thompson Seedless (TS) expressing ether CAP or PGIP were tested in the greenhouse and those lines that showed resistance to PD were grafted with wild type TS scions. Grafted grapevines were introduced into the field and tested over 7 years. Here we present data on the field evaluation of trans-graft protection using four CAP and four PGIP independent rootstock lines, compared to an untransformed rootstock. There was 30 to 95% reduction in vine mortality among CAP- and PGIP-expressing lines after three successive yearly infections with virulent Xf. Shoot tissues grafted to either CAP or PGIP transgenic rootstocks supported lower pathogen titers and showed fewer disease symptoms. Grafted plants on transgenic rootstocks also had more spring bud break following infection, more shoots, and more vigorous growth compared to those grafted to wild type rootstocks. No yield penalty was observed in the transgenic lines and some PGIP-expressing vines had enhanced yield potential. Trans-graft protection is an efficient way to protect grape scions against PD while preserving their valuable varietal genotypes and clonal properties.

Mutations in pre-mRNA processing factors (PRPFs) cause 40% of autosomal dominant retinitis pigmentosa (RP), but it is unclear why mutations in ubiquitously expressed PRPFs cause retinal disease. To understand the molecular basis of this phenotype, we have generated RP type 11 (PRPF31-mutated) patient-specific retinal organoids and retinal pigment epithelium (RPE) from induced pluripotent stem cells (iPSC). Impaired alternative splicing of genes encoding pre-mRNA splicing proteins occurred in patient-specific retinal cells and Prpf31 /- mouse retinae, but not fibroblasts and iPSCs, providing mechanistic insights into retinal-specific phenotypes of PRPFs. RPE was the most affected, characterised by loss of apical-basal polarity, reduced trans-epithelial resistance, phagocytic capacity, microvilli, and cilia length and incidence. Disrupted cilia morphology was observed in patient-derived-photoreceptors that displayed progressive features associated with degeneration and cell stress. In situ gene-editing of a pathogenic mutation rescued key structural and functional phenotypes in RPE and photoreceptors, providing proof-of-concept for future therapeutic strategies.

SummaryMutations in pre-mRNA processing factors (PRPFs) cause 40% of autosomal dominant retinitis pigmentosa (RP), but it is unclear why mutations in ubiquitously expressed PRPFs cause retinal disease. To understand the molecular basis of this phenotype, we have generated RP type 11 (PRPF31-mutated) patient-specific retinal organoids and retinal pigment epithelium (RPE) from induced pluripotent stem cells (iPSC). Impaired alternative splicing of genes encoding pre-mRNA splicing proteins occurred in patient-specific retinal cells and Prpf31+/− mouse retinae, but not fibroblasts and iPSCs, providing mechanistic insights into retinal-specific phenotypes of PRPFs. RPE was the most affected, characterised by loss of apical-basal polarity, reduced trans-epithelial resistance, phagocytic capacity, microvilli, and cilia length and incidence. Disrupted cilia morphology was observed in patient-derived-photoreceptors that displayed progressive features associated with degeneration and cell stress. In situ gene-editing of a pathogenic mutation rescued key structural and functional phenotypes in RPE and photoreceptors, providing proof-of-concept for future therapeutic strategies.eTOCPRPF31 is a ubiquitously expressed pre-mRNA processing factor that when mutated causes autosomal dominant RP. Using a patient-specific iPSC approach, Buskin and Zhu et al. show that retinal-specific defects result from altered splicing of genes involved in the splicing process itself, leading to impaired splicing, loss of RPE polarity and diminished phagocytic ability as well as reduced cilia incidence and length in both photoreceptors and RPE.HighlightsSuccessful generation of iPSC-derived RPE and photoreceptors from four RP type 11 patientsRPE cells express the mutant PRPF31 protein and show the lowest expression of wildtype proteinPRPF31 mutations result in altered splicing of genes involved in pre-mRNA splicing in RPE and retinal organoidsPrpf31 haploinsufficiency results in altered splicing of genes involved in pre-mRNA splicing in mouse retinaRPE cells display loss of polarity, reduced barrier function and phagocytosisPhotoreceptors display shorter and fewer cilia and degenerative featuresRPE cells display most abnormalities suggesting they might be the primary site of pathogenesisIn situ gene editing corrects the mutation and rescues key phenotypes

MicroRNAs are non-coding RNAs with roles in many cellular processes. Tissue-specific miRNA profiles associated with senescence have been described for several cell and tissue types. We aimed to characterise miRNAs involved in core, rather than tissue-specific, senescence pathways by assessment of common miRNA expression differences in two different cell types, with follow-up of predicted targets in human peripheral blood. MicroRNAs were profiled in early and late passage primary lung and skin fibroblasts to identify commonly-deregulated miRNAs. Expression changes of their bioinformatically-predicted mRNA targets were then assessed in both cell types and in human peripheral blood from elderly participants in the InCHIANTI study. 57/178 and 26/492 microRNAs were altered in late passage skin and lung cells respectively. Three miRNAs (miR-92a, miR-15b and miR-125a-3p) were altered in both tissues. 14 mRNA targets of the common miRNAs were expressed in lung and skin fibroblasts, of which two demonstrated up-regulation in late passage skin and lung cells (LYST; p = 0.02 [skin] and 0.02 [lung] INMT; p = 0.03 [skin] and 0.04 [lung]). ZMPSTE24 and LHFPL2 demonstrated altered expression in late passage skin cells only (p = 0.01 and 0.05 respectively). LHFPL2 was also positively correlated with age in peripheral blood (p value = 6.6 × 10(-5)). We find that the majority of senescence-associated miRNAs demonstrate tissue-specific effects. However, miRNAs showing common effects across tissue types may represent those associated with core, rather than tissue-specific senescence processes.

Pierce’s disease (PD) is a deadly disease of grapevines caused by the Gram-negative bacterium Xylella fastidiosa. Though disease symptoms were formerly attributed to bacteria blocking the plant xylem, this hypothesis is at best overly simplistic. Recently, we used a proteomic approach to characterize the secretome of X. fastidiosa, both in vitro and in planta and identified LesA as one of the pathogenicity factors of X. fastidiosa in grapevines that leads to leaf scorching and chlorosis. Herein, we characterize another such factor encoded by PD0956, designated as an antivirulence secreted protease “PrtA” that displays a central role in controlling in vitro cell proliferation, length, motility, biofilm formation and in planta virulence. The mutant in X. fastidiosa exhibited reduced cell length, hypermotility (and subsequent lack of biofilm formation) and hypervirulence in grapevines. These findings are supported by transcriptomic and proteomic analyses with corresponding plant infection data. Of particular interest, is the hypervirulent response in grapevines observed when X. fastidiosa is disrupted for production of PrtA and that PD-model tobacco plants transformed to express PrtA exhibited decreased symptoms after infection by X. fastidiosa.

Background Huanglongbing (HLB) disease is still the greatest threat to citriculture worldwide. Although there is not any resistance source in the Citrus germplasm, a certain level of moderated tolerance is present. A large-scale analysis of proteomic responses of Citrus may help: 1) clarifying physiological and molecular effects of disease progression, 2) validating previous data at transcriptomic level, and 3) identifying biomarkers for development of early diagnostics, short-term therapeutics and long-term genetic resistance. Results In this work we have conducted a proteomic analysis of mature leaves of two Citrus genotypes with well-known differing tolerances to HLB: Navel orange (highly susceptible) and Volkameriana (moderately tolerant). Pathway enrichment analysis showed that amino acid degradation processes occurred to a larger degree in the Navel orange. No clear differences between the two genotypes were observed for primary metabolic pathways. The most important finding was that four glutathione-S-transferases were upregulated in Volkameriana and not in Navel orange. These proteins are involved in radical ion detoxification. Conclusions Upregulation of proteins involved in radical ion detoxification should be considered as an important mechanism of increased tolerance to HLB. Electronic supplementary material The online version of this article (doi:10.1186/s12870-016-0858-5) contains supplementary material, which is available to authorized users.

Recent studies suggest that dementia in the most elderly (90 years of age and above) is only modestly related to Alzheimer's disease pathology. This raises the possibility that other, as yet unknown, disease processes may underlie dementia in this rapidly growing demographic group, and that efforts designed to combat Alzheimer's disease may not be appropriate for treating dementia in very elderly subjects. To study this question more closely, we examined the relationship between neocortical Alzheimer-type brain pathology and dementia in consecutive autopsies from 209 participants in the Baltimore Longitudinal Study of Ageing, a prospective longitudinal cohort study of the effect of ageing on cognition. Almost half of the cohort was older than 90 years of age at death. We found that several measures of neocortical Alzheimer's pathology, including the Consortium to Establish a Registry of Alzheimer's Disease neuritic plaque score and the Braak neurofibrillary tangle score, remained significant predictors of dementia, independent of age. In participants older than 90 years of age, intracranial atherosclerosis emerged as an important predictor of dementia in subjects with low Alzheimer's pathology scores, but did not mitigate the importance or population attributable risk of high Alzheimer's pathology scores on the odds of dementia. There was evidence that the threshold score for neurofibrillary pathology to cause dementia increased in the oldest subjects, but this was offset by an overall increase in neurofibrillary pathology in this age group. We conclude that neocortical Alzheimer's disease pathology remains significantly correlated with dementia, independent of age. In the most elderly, atherosclerosis also emerged as a cause of dementia in subjects with low Alzheimer's pathology scores. We found no evidence for a significant number of elderly subjects having dementia without an apparent cause.

In 1910, American philosopher William James called on governments of all nations to eschew fighting each other, and instead jointly pursue 'the moral equivalent of war' - a war against nature. Believing the world to be fundamentally hostile to the human struggle for survival, James was inspired by the projects of the great 19th century engineers. He saw their work as a grand cultural endeavour, transcending merely building infrastructure to solve local practical problems. Pipelines, railways, roads, tunnels, bridges and canals tie formerly separate places and people together, creating new political, economic and population zones. The engineers of the Victorian and Edwardian era literally reshaped the landscape and redrew the maps, changing forever the ways we experience, conceptualise and understand the environment. In the context of the British Empire, impressive engineering works were articulated to enhance the credibility of the imperial enterprise. The visual impact on the physical landscape was controversial, but the new spatial and cultural reality they created is reflected in landscape art and popular national imagery. The fame and drama that surrounded C. Y. O'Connor in Australia and New Zealand, and his international peers, made them significant cultural figures in their own right, as influential as literary or visual artists in creating cultural imagery and sense of place.

Several states currently have enacted laws that allow for civil commitment for individuals diagnosed with severe substance use disorders. Civil commitment or involuntary commitment refers to the legal process by which individuals with mental illness are court-ordered into inpatient and/or outpatient treatment programs. Although initially civil commitment laws were intended for individuals with severe mental illness, these statutes have been extended to cover individuals with severe substance use disorders. Much of the recent legislation allowing for civil commitment of individuals with substance use disorders has come about in response to the heroin epidemic and is designed to provide an alternative to the unrelenting progression of opioid use disorders. Civil commitment also provides an opportunity for individuals with opioid use disorders to make informed decisions regarding ongoing or continued treatment. However, civil commitment also raises concerns regarding the potential violation of 14th Amendment rights, specifically pertaining to abuses of deprivation of liberty or freedom, which are guaranteed under the 14th Amendment to the United States Constitution. This commentary examines these issues while supporting the need for effective brief civil commitment legislation in all states.

The late 1997 opening of Frank Gehry's spectacular new Guggenheim in Bilbao has been widely promoted as the international museum event of the decade. In the context of other developments, it has also been seen as evidence of Guggenheim director Thomas Krens's ‘tireless efforts to build the world's first global museum brand’. In post‐colonial countries such as Australia we know that museums have often been inextricably involved in imperial and international as well as national cultural power struggles. In this paper the ‘global brand’ view of the Guggenheim is further examined in an attempt to clarify whether this is just more of the same, (old wine in a new bottle) or whether museums are entering a new era of globalisation—and if so what may be some of the consequences for professional museum practice.

Huanglongbing (HLB; citrus greening) is the most devastating disease of citrus worldwide. No cure is yet available for this disease and infected trees generally decline after several months. Disease management depends on early detection of symptoms and chemical control of insect vectors. In this work, different combinations of organic compounds were tested for the ability to modulate citrus molecular responses to HLB disease beneficially. Three small-molecule regulating compounds were tested: 1) L-arginine, 2) 6-benzyl-adenine combined with gibberellins, and 3) sucrose combined with atrazine. Each treatment contained K-phite mineral solution and was tested at two different concentrations. Two trials were conducted: one in the greenhouse and the other in the orchard. In the greenhouse study, responses of 42 key genes involved in sugar and starch metabolism, hormone-related pathways, biotic stress responses, and secondary metabolism in treated and untreated mature leaves were analyzed. TGA5 was significantly induced by arginine. Benzyladenine and gibberellins enhanced two important genes involved in biotic stress responses: WRKY54 and WRKY59. Sucrose combined with atrazine mainly upregulated key genes involved in carbohydrate metabolism such as sucrose-phosphate synthase, sucrose synthase, starch synthase, and α-amylase. Atrazine also affected expression of some key genes involved in systemic acquired resistance such as EDS1, TGA6, WRKY33, and MYC2. Several treatments upregulated HSP82, which might help protect protein folding and integrity. A subset of key genes was chosen as biomarkers for molecular responses to treatments under field conditions. GPT2 was downregulated by all small-molecule treatments. Arginine-induced genes involved in systemic acquired resistance included PR1, WRKY70, and EDS1. These molecular data encourage long-term application of treatments that combine these regulating molecules in field trials.

Blackouts are serious. They can lead to heavy loss of industrial production and expose people to precarious situations. One will find many publications on the subject as early as the eighties. It has been and is still today a preoccupation of market regulators and company managers. At Hydro-Quebec, several network upgrades have been made to avoid such an event and the RECRE system has been in production since 2006 to respond adequately in the event of a blackout. In this paper, we present the next generation of the RECRE system. It is CIM based, capable of ensuring real-time accuracy of the restoration plan and to provide an OTS exclusively dedicated to performing power system restoration drills.

David Dolan reviews Yesterday’s Tomorrows: The Powerhouse Museum and its Predecessors , edited by Graeme Davison and Kimberley Webber (Sydney: Powerhouse Publishing and UNSW Press; 2005, pp.288. AU $54.96).

The preferential coordination of primary amines to the copper-EDTA complex and the resulting fall in absorbance at 720 mμ is used as a basis for the accurate determination of both primary and tertiary amines in mixed aqueous solutions.The total amine content is first determined by spectrophotoimetric titration of the mixed amine solution with the dibasic copper-EDTA complex (or vice versa). Then the mixed solution of amines is diluted to a definite total amine concentration, and its absorbance at 720 mμ is again measured after the addition of a definite amount of the tetrasodium salt of EDTA complexed with copper, (CuY)2-. This absorbance is located on a suitable varying concentration ratio curve, and the concentrations of both primary and tertiary amines in the solution being analyzed can be read directly from the curve.

La deuxième moitié du vingtième siècle a vu un changement marqué dans la manière de présenter, de collectionner et de comprendre l’art des peuples indigènes d’Australie. Les approches antérieures spécialisées (ethnographique et anthropologique) des artefacts aborigènes ont été remplacées par la reconnaissance générale que l’art indigène (qui offre des formes nouvelles souvent proches de l’art contemporain) n’est pas seulement un élément important et unique de l’art de l’Australie moderne, mais en constitue évidement l’aspect le plus intéressant pour le reste du monde. On sait que les attitudes et les pratiques institutionnelles se sont transformées au cours des années 1970 et 1980. Dans le contexte d’un lent abandon d’une histoire lourde de politiques culturelles racistes, ces décennies constituaient un intervalle entre les premières réformes des années 1960, au moment où les aborigènes australiens eurent accès – tardivement – à la pleine citoyenneté, et les années 1990 alors que la « Réconciliation » entre les peuples indigènes et les descendants des colons devint un enjeu politique de premier plan. Au début de XXIe siècle, les productions des artistes aborigènes obtiennent les plus hautes cotes du marché de l’art, bien supérieures à ce que pouvait obtenir les autres artistes vivants. Cet article s’interroge sur le rôle de la recherche et de l’enseignement universitaires dans la réévaluation de l’art aborigène de la culture australienne contemporaine. Nous croyons que l’histoire de l’art et les cours théoriques universitaires, le milieu du marché de l’art ainsi que les principaux musées d’art publics ont tous eu un rôle à jouer dans la transformation du statut de l’art aborigène, mais que l’université s’est contentée de suivre le mouvement avec les autres instances, plutôt que d’en montrer la voie.

The recent re-introduction of improvisation as a professional practice within classical music, however cautious and still rare, allows direct and detailed contemporary comparison between improvised and "standard" approaches to performances of the same composition, comparisons which hitherto could only be inferred from impressionistic historical accounts. This study takes an interdisciplinary multi-method approach to discovering the contrasting nature and effects of prepared and improvised approaches during live chamber-music concert performances of a movement from Franz Schubert's "Shepherd on the Rock," given by a professional trio consisting of voice, flute, and piano, in the presence of an invited audience of 22 adults with varying levels of musical experience and training. The improvised performances were found to differ systematically from prepared performances in their timing, dynamic, and timbral features as well as in the degree of risk-taking and "mind reading" between performers, which included moments of spontaneously exchanging extemporized notes. Post-performance critical reflection by the performers characterized distinct mental states underlying the two modes of performance. The amount of overall body movements was reduced in the improvised performances, which showed less unco-ordinated movements between performers when compared to the prepared performance. Audience members, who were told only that the two performances would be different, but not how, rated the improvised version as more emotionally compelling and musically convincing than the prepared version. The size of this effect was not affected by whether or not the audience could see the performers, or by levels of musical training. EEG measurements from 19 scalp locations showed higher levels of Lempel-Ziv complexity (associated with awareness and alertness) in the improvised version in both performers and audience. Results are discussed in terms of their potential support for an "improvisatory state of mind" which may have aspects of flow (as characterized by Csikszentmihalyi, 1997) and primary states (as characterized by the Entropic Brain Hypothesis of Carhart-Harris et al., 2014). In a group setting, such as a live concert, our evidence suggests that this state of mind is communicable between performers and audience thus contributing to a heightened quality of shared experience.