What controls the vertical distribution of aerosol? Relationships between process sensitivity in HadGEM3–UKCA and inter-model variation from AeroCom Phase II

The vertical profile of aerosol is important for its radiative effects, but weakly constrained by observations on the global scale, and highly variable among different models. To investigate the controlling factors in one particular model, we investigate the effects of individual processes in HadGEM3–UKCA and compare the resulting diversity of aerosol vertical profiles with the inter-model diversity from the AeroCom Phase II control experiment. In this way we show that (in this model at least) the vertical profile is controlled by a relatively small number of processes, although these vary among aerosol components and particle sizes. We also show that sufficiently coarse variations in these processes can produce a similar diversity to that among different models in terms of the global-mean profile and, to a lesser extent, the zonal-mean vertical position. However, there are features of certain models' profiles that cannot be reproduced, suggesting the influence of further structural differences between models. In HadGEM3–UKCA, convective transport is found to be very important in controlling the vertical profile of all aerosol components by mass. In-cloud scavenging is very important for all except mineral dust. Growth by condensation is important for sulfate and carbonaceous aerosol (along with aqueous oxidation for the former and ageing by soluble material for the latter). The vertical extent of biomass-burning emissions into the free troposphere is also important for the profile of carbonaceous aerosol. Boundary-layer mixing plays a dominant role for sea salt and mineral dust, which are emitted only from the surface. Dry deposition and below-cloud scavenging are important for the profile of mineral dust only. In this model, the microphysical processes of nucleation, condensation and coagulation dominate the vertical profile of the smallest particles by number (e.g. total CN  >  3 nm), while the profiles of larger particles (e.g. CN  >  100 nm) are controlled by the same processes as the component mass profiles, plus the size distribution of primary emissions. We also show that the processes that affect the AOD-normalised radiative forcing in the model are predominantly those that affect the vertical mass distribution, in particular convective transport, in-cloud scavenging, aqueous oxidation, ageing and the vertical extent of biomass-burning emissions.

Acoustic features involved in the neighbour-stranger vocal recognition process in male Australian fur seals

Many territorial species have the ability to recognise neighbours from stranger individuals. If the neighbouring individual is assumed to pose less of a threat, the territorial individual responds less and avoids unnecessary confrontations with familiar individuals at established boundaries, thus avoiding the costly energy expenditure associated with fighting. Territorial male Australian fur seals respond more to strangers than to neighbouring males. The present study evaluated which acoustic features were important in the neighbour–stranger recognition process in male Australian fur seals. The results reveal that there was an increase in response strength or intensity from males when they heard more bark units, indicating the importance of repetition to detect a caller. However, lengthening and shortening the inter-unit spaces, (i.e. changing the rhythm of the call) did not appear to significantly affect an animal's response. In addition, the whole frequency spectrum was considered important to recognition with results suggesting that they may vary in their importance. A call containing the dominant and surrounding harmonics was considered important to a male's ability to recognise its neighbour. Furthermore, recognition occurs even with a partial bark, but males need to hear between 25 and 75% of each bark unit from neighbouring seals. Our study highlights which acoustic features induce stronger or weaker responses from territorial males, decoding the important features in neighbour–stranger recognition.

Emptiness and becoming : integrating Madhyamika Buddhism and process philosophy

Beginning with a comparison of process philosophy and Madhyamika Buddhism -focussing in particular on Charles Hartshorne and Nagarjuna - which seeks to find points of similarity and difference, this thesis goes on to ask whether the differences are disagreements or complementary insights that may be integrated by means of a hermeneutical framework which can facilitate the enrichment of both systems. It is argued that process philosophy's method of creative synthesis and Madhyamika's method of negative dialectics are complementary rather than rival methods, because: (1) the Madhyamika bi-negation of symmetrical internal and external relations is complemented by process philosophy's argument that asymmetrical relations have primacy, which can be integrated into a theory of 'asymmetrical interdependence'; (2) the Madhyamika bi-negation of being and non-being is complemented by process philosophy's argument that becoming has primacy; (3) Madhyamika's emptiness (or openness) and process philosophy's creativity are complementary ideas that can be integrated into a ‘creative emptiness’; (4) Madhyamika's deconstruction of theism and acceptance of a conventional (and thus empty) ‘Cosmic Buddha-Bodhisattva’ and process philosophy's panentheism are complementary and can be integrated in the idea of an ‘empty God’; (5) The creative emptiness and the empty God are two different but complementary ultimates - the ultimate activity and the ultimate actuality; (6) Madhyamika’s two truths -conventional (empty world) and ultimate (emptiness) - can be enriched by expanding the conventional to include ultimate actuality (empty God), and not subordinating the conventional to the ultimate; (7) process philosophy can be similarly enriched by meditating on creative emptiness, which reveals the empty God-world, which is not dominant vis-a-vis creative emptiness. An attempt is made to develop a hermeneutical framework for the comparison and integration of Madhyamika and process thought, which can also be used to construct a general theory of worldviews and a theory of interreligious dialogue. Finally, the practical applications of the integration of process thought and Madhyamika Buddhism are explored, focussing on ethical and socio-political issues and how the integration of the two systems can be used to advantage in these contexts.

A panel error correction approach to explore spatial correlation patterns of the dominant housing market in Australian capital cities

Purpose - A panel error correction model has been developed to investigate the spatial correlation patterns among house prices. This paper aims to identify a dominant housing market in the ripple down process. Design/methodology/approach - Seemingly unrelated regression estimators are adapted to deal with the contemporary correlations and heterogeneity across cities. Impulse response functions are subsequently implemented to simulate the spatial correlation patterns. The newly developed approach is then applied to the Australian capital city house price indices. Findings - The results suggest that Melbourne should be recognised as the dominant housing market. Four levels were classified within the Australian house price interconnections, namely: Melbourne; Adelaide, Canberra, Perth and Sydney; Brisbane and Hobart; and Darwin. Originality/value - This research develops a panel regression framework in addressing the spatial correlation patterns of house prices across cities. The ripple-down process of house price dynamics across cities was explored by capturing both the contemporary correlations and heterogeneity, and by identifying the dominant housing market.

The influence of residual stress on a roll forming process

Roll forming is increasingly used in the automotive industry to form High Strength Steel (HSS) and Advanced High Strength Steel (AHSS) for structural components. Because of the large variety of applications of roll forming in the industry, Finite Element Analysis (FEA) is increasingly utilized for roll forming process design. Bending is the dominant deformation mode in roll forming and sheet materials used in the process are often temper rolled (skin passed), roller- or tension-levelled. These processes introduce residual stresses into the material, and recent studies have shown that those affect the material behaviour in bending. A thickness reduction rolling process available at Deakin that leads to material deformation similar to an industrial temper rolling operation was used in this study to introduce residual stresses into a dual phase, DP780, steel strip. The initial and thickness reduced strips were then used in a 5-stand experimental V-section roll forming set-up to identify the effect of residual stress on the final shape. The influence of residual stress and the effect of plastic deformation on the material behaviour in roll forming are separately determined in numerical simulation. The results show that the thickness reduction rolling process decreases the maximum bow height while the springback angle and end flare increase. Comparison with experimental results shows that using material data from the conventional tensile test in a numerical simulation does not allow for the accurate prediction of shape defects in a roll forming process if a residual stress profile exists in the material. On the other hand including the residual stress information leads to improved model accuracy.

Decision making process: a comparison between the public and private sector

The problem of decision making, its mechanisms and consequences is the very core of management, it is virtually impossible to separate the act of manage from this knowledge area. As defined by Herbert Simon – "decision making" as though it were synonymous with "managing". A decision is a selection made by an individual regarding a choice of a conclusion about a situation. This represents a course of behavior pertaining to what must be done or what must not be done. A decision is the point at which plans, policies and objectives are translated into concrete actions. Our behavior during decisive moments is closely linked with our brain dominance profile. Over the years, our decision-making processes develop a consistent pattern, which can be described as a decision-making style. Our style is grounded in our preferences, which arise from our brain dominance characteristics […]. The importance of understanding the impact of our thinking preferences and how to improve the effectiveness as a leader of organizations are the main justifications for this thesis; the main problem addressed is the behavioral profile diversity in a selective Master’s cohort formed by students from several different countries. The research methodology approach has been quantitative, through questionnaire administration using the HBDI (Herrmann Brain Dominance Instrument), a validated framework developed by William "Ned" Herrmann when he was the leader of General Electric's Crotonville facility. This questionnaire has been administered in hundreds of thousands professional, enabling the possibility to establish correlations between a certain group and several historical databases. The selected group of analysis is the first cohort (23 students) from the CIM (Corporate International Master's), a joint program between Georgetown University (USA), ESADE (Spain) and FGV (Brazil). Besides decision preferences, the obtained profile enables the discussion on leadership style, heuristic's pitfalls and a base to compare with future cohorts. The fundamental research question is: how diverse is the dominant decision-making profile for the CIM students?

Measurement of the weak mixing angle with the Drell-Yan process in proton-proton collisions at the LHC

Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

Study of the annealing temperature effect on the structural and luminescent properties of SrWO4:Eu phosphors prepared by a non-hydrolytic sol-gel process

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

EX-SITU BIOREMEDIATION OF BRAZILIAN SOIL CONTAMINATED WITH PLASTICIZERS PROCESS WASTES

The aim of this research was to evaluate the bioremediation of a soil contaminated with wastes from a plasticizers industry, located in Sao Paulo, Brazil. A 100-kg soil sample containing alcohols, adipates and phthalates was treated in an aerobic slurry-phase reactor using indigenous and acclimated microorganisms from the sludge of a wastewater treatment plant of the plasticizers industry (11gVSS kg(-1) dry soil), during 120 days. The soil pH and temperature were not corrected during bioremediation; soil humidity was corrected weekly to maintain 40%. The biodegradation of the pollutants followed first-order kinetics; the removal efficiencies were above 61% and, among the analyzed plasticizers, adipate was removed to below the detection limit. Biological molecular analysis during bioremediation revealed a significant change in the dominant populations initially present in the reactor.

Ex-situ bioremediation of Brazilian soil contaminated with plasticizers process wastes

The aim of this research was to evaluate the bioremediation of a soil contaminated with wastes from a plasticizers industry, located in São Paulo, Brazil. A 100-kg soil sample containing alcohols, adipates and phthalates was treated in an aerobic slurry-phase reactor using indigenous and acclimated microorganisms from the sludge of a wastewater treatment plant of the plasticizers industry (11gVSS kg-1 dry soil), during 120 days. The soil pH and temperature were not corrected during bioremediation; soil humidity was corrected weekly to maintain 40%. The biodegradation of the pollutants followed first-order kinetics; the removal efficiencies were above 61% and, among the analyzed plasticizers, adipate was removed to below the detection limit. Biological molecular analysis during bioremediation revealed a significant change in the dominant populations initially present in the reactor.

Studies of OPA1 pathogenic mechanisms in Dominant Optic Atrophy and novel protein function in mitochondrial DNA stability

The mitochondrion is an essential cytoplasmic organelle that provides most of the energy necessary for eukaryotic cell physiology. Mitochondrial structure and functions are maintained by proteins of both mitochondrial and nuclear origin. These organelles are organized in an extended network that dynamically fuses and divides. Mitochondrial morphology results from the equilibrium between fusion and fission processes, controlled by a family of “mitochondria-shaping” proteins. It is becoming clear that defects in mitochondrial dynamics can impair mitochondrial respiration, morphology and motility, leading to apoptotic cell death in vitro and more or less severe neurodegenerative disorders in vivo in humans. Mutations in OPA1, a nuclear encoded mitochondrial protein, cause autosomal Dominant Optic Atrophy (DOA), a heterogeneous blinding disease characterized by retinal ganglion cell degeneration leading to optic neuropathy (Delettre et al., 2000; Alexander et al., 2000). OPA1 is a mitochondrial dynamin-related guanosine triphosphatase (GTPase) protein involved in mitochondrial network dynamics, cytochrome c storage and apoptosis. This protein is anchored or associated on the inner mitochondrial membrane facing the intermembrane space. Eight OPA1 isoforms resulting from alternative splicing combinations of exon 4, 4b and 5b have been described (Delettre et al., 2001). These variants greatly vary among diverse organs and the presence of specific isoforms has been associated with various mitochondrial functions. The different spliced exons encode domains included in the amino-terminal region and contribute to determine OPA1 functions (Olichon et al., 2006). It has been shown that exon 4, that is conserved throughout evolution, confers functions to OPA1 involved in maintenance of the mitochondrial membrane potential and in the fusion of the network. Conversely, exon 4b and exon 5b, which are vertebrate specific, are involved in regulation of cytochrome c release from mitochondria, and activation of apoptosis, a process restricted to vertebrates (Olichon et al., 2007). While Mgm1p has been identified thanks to its role in mtDNA maintenance, it is only recently that OPA1 has been linked to mtDNA stability. Missense mutations in OPA1 cause accumulation of multiple deletions in skeletal muscle. The syndrome associated to these mutations (DOA-1 plus) is complex, consisting of a combination of dominant optic atrophy, progressive external ophtalmoplegia, peripheral neuropathy, ataxia and deafness (Amati- Bonneau et al., 2008; Hudson et al., 2008). OPA1 is the fifth gene associated with mtDNA “breakage syndrome” together with ANT1, PolG1-2 and TYMP (Spinazzola et al., 2009). In this thesis we show for the first time that specific OPA1 isoforms associated to exon 4b are important for mtDNA stability, by anchoring the nucleoids to the inner mitochondrial membrane. Our results clearly demonstrate that OPA1 isoforms including exon 4b are intimately associated to the maintenance of the mitochondrial genome, as their silencing leads to mtDNA depletion. The mechanism leading to mtDNA loss is associated with replication inhibition in cells where exon 4b containing isoforms were down-regulated. Furthermore silencing of exon 4b associated isoforms is responsible for alteration in mtDNA-nucleoids distribution in the mitochondrial network. In this study it was evidenced that OPA1 exon 4b isoform is cleaved to provide a 10kd peptide embedded in the inner membrane by a second transmembrane domain, that seems to be crucial for mitochondrial genome maintenance and does correspond to the second transmembrane domain of the yeasts orthologue encoded by MGM1 or Msp1, which is also mandatory for this process (Diot et al., 2009; Herlan et al., 2003). Furthermore in this thesis we show that the NT-OPA1-exon 4b peptide co-immuno-precipitates with mtDNA and specifically interacts with two major components of the mitochondrial nucleoids: the polymerase gamma and Tfam. Thus, from these experiments the conclusion is that NT-OPA1- exon 4b peptide contributes to the nucleoid anchoring in the inner mitochondrial membrane, a process that is required for the initiation of mtDNA replication and for the distribution of nucleoids along the network. These data provide new crucial insights in understanding the mechanism involved in maintenance of mtDNA integrity, because they clearly demonstrate that, besides genes implicated in mtDNA replications (i.e. polymerase gamma, Tfam, twinkle and genes involved in the nucleotide pool metabolism), OPA1 and mitochondrial membrane dynamics play also an important role. Noticeably, the effect on mtDNA is different depending on the specific OPA1 isoforms down-regulated, suggesting the involvement of two different combined mechanisms. Over two hundred OPA1 mutations, spread throughout the coding region of the gene, have been described to date, including substitutions, deletions or insertions. Some mutations are predicted to generate a truncated protein inducing haploinsufficiency, whereas the missense nucleotide substitutions result in aminoacidic changes which affect conserved positions of the OPA1 protein. So far, the functional consequences of OPA1 mutations in cells from DOA patients are poorly understood. Phosphorus MR spectroscopy in patients with the c.2708delTTAG deletion revealed a defect in oxidative phosphorylation in muscles (Lodi et al., 2004). An energetic impairment has been also show in fibroblasts with the severe OPA1 R445H mutation (Amati-Bonneau et al., 2005). It has been previously reported by our group that OPA1 mutations leading to haploinsufficiency are associated in fibroblasts to an oxidative phosphorylation dysfunction, mainly involving the respiratory complex I (Zanna et al., 2008). In this study we have evaluated the energetic efficiency of a panel of skin fibroblasts derived from DOA patients, five fibroblast cell lines with OPA1 mutations causing haploinsufficiency (DOA-H) and two cell lines bearing mis-sense aminoacidic substitutions (DOA-AA), and compared with control fibroblasts. Although both types of DOA fibroblasts maintained a similar ATP content when incubated in a glucose-free medium, i.e. when forced to utilize the oxidative phosphorylation only to produce ATP, the mitochondrial ATP synthesis through complex I, measured in digitonin-permeabilized cells, was significantly reduced in cells with OPA1 haploinsufficiency only, whereas it was similar to controls in cells with the missense substitutions. Furthermore, evaluation of the mitochondrial membrane potential (DYm) in the two fibroblast lines DOA-AA and in two DOA-H fibroblasts, namely those bearing the c.2819-2A>C mutation and the c.2708delTTAG microdeletion, revealed an anomalous depolarizing response to oligomycin in DOA-H cell lines only. This finding clearly supports the hypothesis that these mutations cause a significant alteration in the respiratory chain function, which can be unmasked only when the operation of the ATP synthase is prevented. Noticeably, oligomycin-induced depolarization in these cells was almost completely prevented by preincubation with cyclosporin A, a well known inhibitor of the permeability transition pore (PTP). This results is very important because it suggests for the first time that the voltage threshold for PTP opening is altered in DOA-H fibroblasts. Although this issue has not yet been addressed in the present study, several are the mechanisms that have been proposed to lead to PTP deregulation, including in particular increased reactive oxygen species production and alteration of Ca2+ homeostasis, whose role in DOA fibroblasts PTP opening is currently under investigation. Identification of the mechanisms leading to altered threshold for PTP regulation will help our understanding of the pathophysiology of DOA, but also provide a strategy for therapeutic intervention.

Interplay Between Finite Resources and a Local Defect in an Asymmetric Simple Exclusion Process

When particle flux is regulated by multiple factors such as particle supply and varying transport rate, it is important to identify the respective dominant regimes. We extend the well-studied totally asymmetric simple exclusion model to investigate the interplay between a controlled entrance and a local defect site. The model mimics cellular transport phenomena where there is typically a finite particle pool and nonuniform moving rates due to biochemical kinetics. Our simulations reveal regions where, despite an increasing particle supply, the current remains constant while particles redistribute in the system. Exploiting a domain wall approach with mean-field approximation, we provide a theoretical ground for our findings. The results in steady-state current and density profiles provide quantitative insights into the regulation of the transcription and translation process in bacterial protein synthesis.

A pedigree with autosomal dominant thrombocytopenia, red cell macrocytosis, and an occurrence of t(12:21) positive pre-B acute lymphoblastic leukemia

Sampling and analyzing new families with inherited blood disorders are major steps contributing to the identification of gene(s) responsible for normal and pathologic hematopoiesis. Familial occurrences of hematological disorders alone, or as part of a syndromic disease, have been reported, and for some the underlying genetic mutation has been identified. Here we describe a new autosomal dominant inherited phenotype of thrombocytopenia and red cell macrocytosis in a four-generation pedigree. Interestingly, in the youngest generation, a 2-year-old boy presenting with these familial features has developed acute lymphoblastic leukemia characterized by a t(12;21) translocation. Tri-lineage involvement of platelets, red cells and white cells may suggest a genetic defect in an early multiliear progenitor or a stem cell. Functional assays in EBV-transformed cell lines revealed a defect in cell proliferation and tubulin dynamics. Two candidate genes, RUNX1 and FOG1, were sequenced but no pathogenic mutation was found. Identification of the underlying genetic defect(s) in this family may help in understanding the complex process of hematopoiesis.

Tree phenology and carbon dioxide fluxes - use of digital photography for process-based interpretation at the ecosystem scale

Vegetation phenology is an important indicator of climate change and climate variability and it is strongly connected to biospheric–atmospheric gas exchange. We aimed to evaluate the applicability of phenological information derived from digital imagery for the interpretation of CO2 exchange measurements. For the years 2005–2007 we analyzed seasonal phenological development of 2 temperate mixed forests using tower-based imagery from standard RGB cameras. Phenological information was jointly analyzed with gross primary productivity (GPP) derived from net ecosystem exchange data. Automated image analysis provided reliable information on vegetation developmental stages of beech and ash trees covering all seasons. A phenological index derived from image color values was strongly correlated with GPP, with a significant mean time lag of several days for ash trees and several weeks for beech trees in early summer (May to mid-July). Leaf emergence dates for the dominant tree species partly explained temporal behaviour of spring GPP but were also masked by local meteorological conditions. We conclude that digital cameras at flux measurement sites not only provide an objective measure of the physiological state of a forest canopy at high temporal and spatial resolutions, but also complement CO2 and water exchange measurements, improving our knowledge of ecosystem processes.

Chromosomal control of the dominant suppression of {\it ras\/}-mediated transformation

The role of tumor suppressor function in the multistep process of carcinogenesis was studied in the human teratocarcinoma cell line PA-1. Early passage PA-1 cells ($<$P100) are preneoplastic while late passage ($>$P100) PA-1 cells are spontaneously transformed. Previous work demonstrated a causal role for the N-ras oncogene in the neoplastic transformation of this cell line and the gene was cloned. A clonal cell line established at passage 40 has been shown to suppress the neoplastic transformation potential of the PA-1 N-ras oncogene in gene transfer experiments. This phenotype has been termed SRT+ for suppression of ras transformation. A clonal cell line established at passage 63 is neoplastically transformed by the N-ras in similar gene transfer experiments and is regarded as srt$-$. Somatic cell hybrids were formed between the SRT+ cell and two different N-ras transformed srt$-$ cells. The results indicate that five of the seven independent hybrid clones, and all 14 subclones, failed to form tumors in the nude mouse tumor assay. Chromosomal analysis of rare neoplastic segregants which arose from suppressed hybrid populations demonstrate that the general loss of chromosomes correlates with the reemergence of neoplastic transformation. Karyotype analyses demonstrate a statistically correlative loss of chromosomes 1, 4, 19, and to a lesser extent 11, 14, and 16. DNA hybridization analysis demonstrates a single copy of the intact N-ras oncogene in parental cells, suppressed hybrids, and neoplastically transformed hybrids. These results indicate that functional ras transformation suppression is a trans-dominant trait which may be controlled by sequences residing on particular chromosomes in the human genome. Furthermore, the suppression of ras transformation results from a unique step in the multistep process of carcinogenesis that is different from the induction of immortality. Thus, the neoplastic process of the PA-1 cell line involves at least three steps: (1) induction of immortality, (2) activation of the N-ras oncogene, and (3) loss of tumor suppressor function. ^