539 research outputs found

    Synoptic relationships between surface Chlorophyll-<i>a</i> and diagnostic pigments specific to phytoplankton functional types

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    Error-quantified, synoptic-scale relationships between chlorophyll-<i>a</i> (Chl-<i>a</i>) and phytoplankton pigment groups at the sea surface are presented. A total of ten pigment groups were considered to represent three Phytoplankton Size Classes (PSCs, micro-, nano- and picoplankton) and seven Phytoplankton Functional Types (PFTs, i.e. diatoms, dinoflagellates, green algae, prymnesiophytes (haptophytes), pico-eukaryotes, prokaryotes and <i>Prochlorococcus</i> sp.). The observed relationships between Chl-<i>a</i> and PSCs/PFTs were well-defined at the global scale to show that a community shift of phytoplankton at the basin and global scales is reflected by a change in Chl-<i>a</i> of the total community. Thus, Chl-<i>a</i> of the total community can be used as an index of not only phytoplankton biomass but also of their community structure. Within these relationships, we also found non-monotonic variations with Chl-<i>a</i> for certain pico-sized phytoplankton (pico-eukaryotes, Prokaryotes and <i>Prochlorococcus</i> sp.) and nano-sized phytoplankton (Green algae, prymnesiophytes). The relationships were quantified with a least-square fitting approach in order to enable an estimation of the PFTs from Chl-<i>a</i> where PFTs are expressed as a percentage of the total Chl-<i>a</i>. The estimated uncertainty of the relationships depends on both PFT and Chl-<i>a</i> concentration. Maximum uncertainty of 31.8% was found for diatoms at Chl-<i>a</i> = 0.49 mg m<sup>−3</sup>. However, the mean uncertainty of the relationships over all PFTs was 5.9% over the entire Chl-<i>a</i> range observed in situ (0.02 &lt; Chl-<i>a</i> &lt; 4.26 mg m<sup>&minus;3</sup>). The relationships were applied to SeaWiFS satellite Chl-<i>a</i> data from 1998 to 2009 to show the global climatological fields of the surface distribution of PFTs. Results show that microplankton are present in the mid and high latitudes, constituting only ~10.9% of the entire phytoplankton community in the mean field for 1998–2009, in which diatoms explain ~7.5%. Nanoplankton are ubiquitous throughout the global surface oceans, except the subtropical gyres, constituting ~45.5%, of which prymnesiophytes (haptophytes) are the major group explaining ~31.7% while green algae contribute ~13.9%. Picoplankton are dominant in the subtropical gyres, but constitute ~43.6% globally, of which prokaryotes are the major group explaining ~26.5% (<i>Prochlorococcus</i> sp. explaining 22.8%), while pico-eukaryotes explain ~17.2% and are relatively abundant in the South Pacific. These results may be of use to evaluate global marine ecosystem models

    Drivers and uncertainties of future global marine primary production in marine ecosystem models

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    Past model studies have projected a global decrease in marine net primary production (NPP) over the 21st century, but these studies focused on the multi-model mean rather than on the large inter-model differences. Here, we analyze model-simulated changes in NPP for the 21st century under IPCC's high-emission scenario RCP8.5. We use a suite of nine coupled carbon–climate Earth system models with embedded marine ecosystem models and focus on the spread between the different models and the underlying reasons. Globally, NPP decreases in five out of the nine models over the course of the 21st century, while three show no significant trend and one even simulates an increase. The largest model spread occurs in the low latitudes (between 30° S and 30° N), with individual models simulating relative changes between −25 and +40 %. Of the seven models diagnosing a net decrease in NPP in the low latitudes, only three simulate this to be a consequence of the classical interpretation, i.e., a stronger nutrient limitation due to increased stratification leading to reduced phytoplankton growth. In the other four, warming-induced increases in phytoplankton growth outbalance the stronger nutrient limitation. However, temperature-driven increases in grazing and other loss processes cause a net decrease in phytoplankton biomass and reduce NPP despite higher growth rates. One model projects a strong increase in NPP in the low latitudes, caused by an intensification of the microbial loop, while NPP in the remaining model changes by less than 0.5 %. While models consistently project increases NPP in the Southern Ocean, the regional inter-model range is also very substantial. In most models, this increase in NPP is driven by temperature, but it is also modulated by changes in light, macronutrients and iron as well as grazing. Overall, current projections of future changes in global marine NPP are subject to large uncertainties and necessitate a dedicated and sustained effort to improve the models and the concepts and data that guide their developmen

    Bridging the gap between omics and earth system science to better understand how environmental change impacts marine microbes

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    The advent of genomic-, transcriptomic- and proteomic-based approaches has revolutionized our ability to describe marine microbial communities, including biogeography, metabolic potential and diversity, mechanisms of adaptation, and phylogeny and evolutionary history. New interdisciplinary approaches are needed to move from this descriptive level to improved quantitative, process-level understanding of the roles of marine microbes in biogeochemical cycles and of the impact of environmental change on the marine microbial ecosystem. Linking studies at levels from the genome to the organism, to ecological strategies and organism and ecosystem response, requires new modelling approaches. Key to this will be a fundamental shift in modelling scale that represents micro-organisms from the level of their macromolecular components. This will enable contact with omics data sets and allow acclimation and adaptive response at the phenotype level (i.e. traits) to be simulated as a combination of fitness maximization and evolutionary constraints. This way forward will build on ecological approaches that identify key organism traits and systems biology approaches that integrate traditional physiological measurements with new insights from omics. It will rely on developing an improved understanding of ecophysiology to understand quantitatively environmental controls on microbial growth strategies. It will also incorporate results from experimental evolution studies in the representation of adaptation. The resulting ecosystem-level models can then evaluate our level of understanding of controls on ecosystem structure and function, highlight major gaps in understanding and help prioritize areas for future research programs. Ultimately, this grand synthesis should improve predictive capability of the ecosystem response to multiple environmental drivers

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    背景 近年, 乳幼児虐待予防の観点から産後ケア事業が注目されている. A県のB病院は, 産後ケア入院事業を開設したが, 利用者が少なく事業目的が果たせていない現状である.目的 産後4ヶ月までの育児サポート状況を明確化し, A県B病院の産後ケア入院の課題について考察することを目的とする.方法 産後4ヶ月から1年未満の母親37名を対象に, 産後4ヶ月までのサポート状況と満足度, 専門家に望むサポート, 産後ケア入院に関する質問紙調査を行った.結果および考察 産後1ヶ月までの主な育児サポート者は実母82.9%, 夫68.6%で, 満足群は95.1%であった. 産後1ヶ月以降は, 夫85.7%, 実母94.3%で, サポート者なしが2.9%で, 満足群は82.9%であったが, 不満足群が2.9%から17.1%に増加したことから, この時期の育児サポートは必要性が高いと考える. 産後ケア入院について 「知らない」 者は62.9%であった. 「知らない」 者のうち50%は 「事前に知っていたら利用した」 と回答しており, 効果的な広報活動が必要である.Background The postpartum care enterprise attracts attention. Although B hospital of A prefecture established the postpartum care hospitalization enterprise, a user is the present condition that the business purpose cannot be achieved few.Objective The childcare support situation by four months of postpartum is clarified, and it aims at considering the subject of postpartum care hospitalization of an A prefectural B hospital.Methods Candidates are 37 mothers for less than one year from four months of postpartum.Results/Discussion The main support persons by one month of postpartum were 82.9% of a biological mother, and 68.6% of a husband, and the satisfactory group was 95.1%. The support persons after one month of postpartum were 85.7% of a husband, and 94.3% of a biological mother, those without a support person were 2.9%, and the satisfactory group was 82.9%. However, the dissatisfied group to child-rearing increased to 17.1% from 2.9%.Therefore, I think that the childcare support after one month of postpartum has high necessity. Next, those who "do not know" postpartum care hospitalization were 62.9%.Since 50% of those who "do not know" postpartum care hospitalization answered, "It used when knowing in advance", it thinks that effective publicity work is required

    IFN-γ signaling, with the synergistic contribution of TNF-α, mediates cell specific microglial and astroglial activation in experimental models of Parkinson's disease

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    To through light on the mechanisms underlying the stimulation and persistence of glial cell activation in Parkinsonism, we investigate the function of IFN-γ and TNF-α in experimental models of Parkinson's disease and analyze their relation with local glial cell activation. It was found that IFN-γ and TNF-α remained higher over the years in the serum and CNS of chronic Parkinsonian macaques than in untreated animals, accompanied by sustained glial activation (microglia and astroglia) in the substantia nigra pars compacta. Importantly, Parkinsonian monkeys showed persistent and increasing levels of IFN-γR signaling in both microglial and astroglial cells. In addition, experiments performed in IFN-γ and TNF-α KO mice treated with MPTP revealed that, even before dopaminergic cell death can be observed, the presence of IFN-γ and TNF-α is crucial for microglial and astroglial activation, and, together, they have an important synergistic role. Both cytokines were necessary for the full level of activation to be attained in both microglial and astroglial cells. These results demonstrate that IFN-γ signaling, together with the contribution of TNF-α, have a critical and cell-specific role in stimulating and maintaining glial cell activation in Parkinsonism

    Artemisinin Attenuates Lipopolysaccharide-Stimulated Proinflammatory Responses by Inhibiting NF-κB Pathway in Microglia Cells

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    Microglial activation plays an important role in neuroinflammation, which contributes to neuronal damage, and inhibition of microglial activation may have therapeutic benefits that could alleviate the progression of neurodegeneration. Recent studies have indicated that the antimalarial agent artemisinin has the ability to inhibit NF-κB activation. In this study, the inhibitory effects of artemisinin on the production of proinflammatory mediators were investigated in lipopolysaccharide (LPS)-stimulated primary microglia. Our results show that artemisinin significantly inhibited LPS-induced production of tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), monocyte chemotactic protein-1 (MCP-1) and nitric oxide (NO). Artemisinin significantly decreased both the mRNA and the protein levels of these pro-inflammatory cytokines and inducible nitric oxide synthase (iNOS) and increased the protein levels of IκB-α, which forms a cytoplasmic inactive complex with the p65-p50 heterodimeric complex. Artemisinin treatment significantly inhibited basal and LPS-induced migration of BV-2 microglia. Electrophoretic mobility shift assays revealed increased NF-κB binding activity in LPS-stimulated primary microglia, and this increase could be prevented by artemisinin. The inhibitory effects of artemisinin on LPS-stimulated microglia were blocked after IκB-α was silenced with IκB-α siRNA. Our results suggest that artemisinin is able to inhibit neuroinflammation by interfering with NF-κB signaling. The data provide direct evidence of the potential application of artemisinin for the treatment of neuroinflammatory diseases

    Molecular changes in the postmortem parkinsonian brain

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    Parkinson disease (PD) is the second most common neurodegenerative disease after Alzheimer disease. Although PD has a relatively narrow clinical phenotype, it has become clear that its etiological basis is broad. Post-mortem brain analysis, despite its limitations, has provided invaluable insights into relevant pathogenic pathways including mitochondrial dysfunction, oxidative stress and protein homeostasis dysregulation. Identification of the genetic causes of PD followed the discovery of these abnormalities, and reinforced the importance of the biochemical defects identified post-mortem. Recent genetic studies have highlighted the mitochondrial and lysosomal areas of cell function as particularly significant in mediating the neurodegeneration of PD. Thus the careful analysis of post-mortem PD brain biochemistry remains a crucial component of research, and one that offers considerable opportunity to pursue etiological factors either by ‘reverse biochemistry’ i.e. from defective pathway to mutant gene, or by the complex interplay between pathways e.g. mitochondrial turnover by lysosomes. In this review we have documented the spectrum of biochemical defects identified in PD post-mortem brain and explored their relevance to metabolic pathways involved in neurodegeneration. We have highlighted the complex interactions between these pathways and the gene mutations causing or increasing risk for PD. These pathways are becoming a focus for the development of disease modifying therapies for PD. Parkinson's is accompanied by multiple changes in the brain that are responsible for the progression of the disease. We describe here the molecular alterations occurring in postmortem brains and classify them as: Neurotransmitters and neurotrophic factors; Lewy bodies and Parkinson's-linked genes; Transition metals, calcium and calcium-binding proteins; Inflammation; Mitochondrial abnormalities and oxidative stress; Abnormal protein removal and degradation; Apoptosis and transduction pathways
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