Interventioner - ett fenomen präglat av kampen mellan maskulint och feminint?

I följande uppsats undersöks frågeställningen: på vilket sätt kan feminismen förklara varför stater intervenerar? Frågeställningen besvaras genom en kvantitativ studie över 186 länder under tidsperioden 1975-2009. Vidare delas frågeställningen upp i två hypoteser: 1) maskulinitet leder till fler interventioner, 2) jämställda länder tenderar att intervenera i mindre utsträckning. Hypoteserna har sin grund i feministisk teori gällande genusdikotomier och sex equality peace. Dessa teorier menar att staters beteende kan förklaras av genus, där maskulina attribut premieras på femininitetens bekostnad. En hög grad av jämställdhet förväntas även leda till fredligare interaktion mellan stater. Vår statistiska analys bekräftar hypotes ett, vilket medför stöd till tidigare forskning. Hypotes två får inget stöd i analysen, utan visar på ett motsatt samband. Resultatet går emot teorier om sex equality peace, men kan möjligen förklaras av state feminism och forskning kring hur normer kan användas för att legitimera interventioner

Chemicals Possessing a Neurotrophin-Like Activity on Dopaminergic Neurons in Primary Culture

BACKGROUND:Neurotrophic factors have been shown to possess strong neuroprotective and neurorestaurative properties in Parkinson's disease patients. However the issues to control their delivery into the interest areas of the brain and their surgical administration linked to their unability to cross the blood brain barrier are many drawbacks responsible of undesirable side effects limiting their clinical use. A strategy implying the use of neurotrophic small molecules could provide an interesting alternative avoiding neurotrophin administration and side effects. In an attempt to develop drugs mimicking neurotrophic factors, we have designed and synthesized low molecular weight molecules that exhibit neuroprotective and neuritogenic potential for dopaminergic neurons. PRINCIPAL FINDINGS:A cell-based screening of an in-house quinoline-derived compound collection led to the characterization of compounds exhibiting both activities in the nanomolar range on mesencephalic dopaminergic neurons in spontaneous or 1-methyl-4-phenylpyridinium (MPP(+))-induced neurodegeneration. This study provides evidence that rescued neurons possess a functional dopamine transporter and underlines the involvement of the extracellular signal-regulated kinase 1/2 signaling pathway in these processes. CONCLUSION:Cell-based screening led to the discovery of a potent neurotrophic compound possessing expected physico-chemical properties for blood brain barrier penetration as a serious candidate for therapeutic use in Parkinson disease

Linking Marine Plankton Ecosystems and Climate:A New Modeling Approach to the Warm Early Eocene Climate

The fossil record reveals large changes in marine plankton ecosystems linked with both environmental and ecological change across the Cenozoic. An understanding of the drivers of these changes is key to understanding the marine carbon cycle. The response of plankton ecosystems in past warm climates also provides a key analogue for current climate change. While models are employed to quantify interactions between the environment and the biota, current Earth system models strongly encode our understanding of modern marine ecosystems. By contrast, trait‐based models aim to describe the marine plankton ecosystem in terms of fundamental ecological and physiological rules that are less likely to change through time. This provides a unique opportunity to assess the interactions between marine ecosystem and paleoclimate. For the first time, we apply a size‐structured trait‐based plankton ecosystem model embedded in the Earth system model of intermediate complexity, cGENIE, to model plankton communities for the warm climate of the early Eocene. Compared to modern, we find the warm climate is associated with an increase in the mean cell size of plankton communities and export production, particularly in the southern high latitudes, along with lower total phytoplankton biomass. Paleogeography has an important role in regulating the effect of ecosystem structure via changes in ocean circulation and nutrient cycling. Warmer temperatures also drive changes due to enhanced zooplankton grazing. An integration of the fossil record with plankton ecosystem models will provide a powerful tool to assess the impacts of warm climates on marine systems

Investigating ocean deoxygenation during the PETM through the Cr isotopic signature of foraminifera

Over the past several decades, oxygen minimum zones have rapidly expanded due to rising temperatures raising concerns about the impacts of future climate change. One way to better understand the drivers behind this expansion is to evaluate the links between climate and seawater deoxygenation in the past especially in times of geologically abrupt climate change such as the Palaeocene-Eocene Thermal Maximum (PETM), a well characterised period of rapid warming ~56 million years ago. We have developed and applied the novel redox proxies of foraminiferal Cr isotopes(δ53Cr) and Ce anomalies (Ce/Ce*) to assess changes in paleo-redox conditions arising from changes in oxygen availability. Both δ53Cr and Cr concentrations decrease notably over the PETM at intermediate to upper abyssal water depths,indicative of widespread reductions in dissolved oxygen concentrations. An apparent correlation between the sizes of δ53Cr and benthic δ18O excursions during the PETM suggests temperature is one of the main controlling factors of deoxygenation in the open ocean. ODP Sites 1210 in the Pacific and 1263 in the Southeast Atlantic suggest that deoxygenation is associated with warming and circulation changes, as supported by Ce/Ce* data. Our geochemical data are supported by simulations from an intermediate complexity climate model (cGENIE), which show that during the PETM anoxia was mostly restricted to the Tethys Sea, while hypoxia was more widespread as a result of increasing atmospheric CO2 (from 1 to 6 times pre-industrial values)

Deltaic and Coastal Sediments as Recorders of Mediterranean Regional Climate and Human Impact Over the Past Three Millennia

This work was financially supported by the MISTRALS/PaleoMex program and by the Project of Strategic Interest NextData PNR 2011–2013 (www. nextdataproject.it). Lionel Savignan is thanked for his participation in the biomarker analysis. Radiocarbon datings for core KESC9-14 have been funded by Institut Carnot Ifremer-EDROME (grant A0811101). We also thank the Holocene North-Atlantic Gyres and Mediterranean Overturning dynamic through Climate Changes (HAMOC) project for financial support. The biomarker data presented here are available in the supporting information.Peer reviewedPublisher PD

Increased Expression of Cytotoxic T-Lymphocyte-Associated Protein 4 by T Cells, Induced by B7 in Sera, Reduces Adaptive Immunity in Patients With Acute Liver Failure.

BACKGROUND & AIMS: Patients with acute liver failure (ALF) have defects in innate immune responses to microbes (immune paresis) and are susceptible to sepsis. Cytotoxic T-lymphocyte-associated protein 4 (CTLA4), which interacts with the membrane receptor B7 (also called CD80 and CD86), is a negative regulator of T-cell activation. We collected T cells from patients with ALF and investigated whether inhibitory signals down-regulate adaptive immune responses in patients with ALF. METHODS: We collected peripheral blood mononuclear cells from patients with ALF and controls from September 2013 through September 2015 (45 patients with ALF, 20 patients with acute-on-chronic liver failure, 15 patients with cirrhosis with no evidence of acute decompensation, 20 patients with septic shock but no cirrhosis or liver disease, and 20 healthy individuals). Circulating CD4+ T cells were isolated and analyzed by flow cytometry. CD4+ T cells were incubated with antigen, or agonist to CD3 and dendritic cells, with or without antibody against CTLA4; T-cell proliferation and protein expression were quantified. We measured levels of soluble B7 molecules in supernatants of isolated primary hepatocytes, hepatic sinusoidal endothelial cells, and biliary epithelial cells from healthy or diseased liver tissues. We also measured levels of soluble B7 serum samples from patients and controls, and mice with acetaminophen-induced liver injury using enzyme-linked immunosorbent assays. RESULTS: Peripheral blood samples from patients with ALF had a higher proportion of CD4+ CTLA4+ T cells than controls; patients with infections had the highest proportions. CD4+ T cells from patients with ALF had a reduced proliferative response to antigen or CD3 stimulation compared to cells from controls; incubation of CD4+ T cells from patients with ALF with an antibody against CTLA4 increased their proliferative response to antigen and to CD3 stimulation, to the same levels as cells from controls. CD4+ T cells from controls up-regulated expression of CTLA4 after 24-48 hours culture with sera from patients with ALF; these sera were found to have increased concentrations of soluble B7 compared to sera from controls. Necrotic human primary hepatocytes exposed to acetaminophen, but not hepatic sinusoidal endothelial cells and biliary epithelial cells from patients with ALF, secreted high levels of soluble B7. Sera from mice with acetaminophen-induced liver injury contained high levels of soluble B7 compared to sera from mice without liver injury. Plasma exchange reduced circulating levels of soluble B7 in patients with ALF and expression of CTLA4 on T cells. CONCLUSIONS: Peripheral CD4+ T cells from patients with ALF have increased expression of CTLA4 compared to individuals without ALF; these cells have a reduced response to antigen and CD3 stimulation. We found sera of patients with ALF and from mice with liver injury to have high concentrations of soluble B7, which up-regulates CTLA4 expression by T cells and reduces their response to antigen. Plasma exchange reduces levels of B7 in sera from patients with ALF and might be used to restore antimicrobial responses to patients

Standard for Synthesis of Customized Peptides by Non-Ribosomal Peptide Synthetases

The purpose of this RFC is to introduce a standardized framework for the engineering of customizable non-ribosomal peptide synthetases (NRPS) and their application for in vivo and in vitro synthesis of short non-ribosomal peptides (NRPs) of user-defined sequence and structure