Cognitive foundations of impartial punitive decision making in organizations: attribution and abstraction

Partial decision making about disciplinary responses to misbehavior is generally considered unfair and undermines the effectiveness of punishment. Nonetheless, organizational actors often struggle to remain impartial in situations that call for punishment. Impartiality appears specifically hard to obtain when some element of the transgression reflects badly upon the punisher themselves, for instance, when in the past the punisher has benefited from the misbehavior, even if just derivatively. In this paper, we argue that in such cases, punishers tend to defensively attribute causes of the transgression to the circumstances in order to protect their own self‐image, thus leading them to relatively lenient punishments. However, we also suggest that psychological impartiality can be obtained through cognitive abstraction. An abstract understanding (high‐level construal) of the punitive situation puts the focus squarely on the gist of the situation and makes circumstantial details less likely to be cognitively available. This hinders defensive circumstantial attribution. We show in a field study and an experiment that partiality in making decisions about punishments occurs under conditions of low‐level (i.e., concrete) construal, whereas impartiality is facilitated by high‐level (i.e., abstract) construal

Role of P-selectin in platelet sequestration in pulmonary capillaries during endotoxemia

Background: There is growing evidence that platelets accumulate in the lung and contribute to the pathogenesis of acute lung injury during endotoxemia. The aims of the present study were to localize platelet sequestration in the pulmonary microcirculation and to investigate the role of P-selectin as a molecular mechanism of platelet endothelial cell interaction. Methods: We used in vivo fluorescence microscopy to quantify the kinetics of fluorescently labeled erythrocytes and platelets in alveolar capillary networks in rabbit lungs. Results: Six hours after onset of endotoxin infusion we observed a massive rolling along and firm adherence of platelets to lung capillary endothelial cells whereas under control conditions no platelet sequestration was detected. P-selectin was expressed on the surface of separated platelets which were incubated with endotoxin and in lung tissue. Pretreatment of platelets with fucoidin, a P-selectin antagonist, significantly attenuated the endotoxin-induced platelet rolling and adherence. In contrast, intravenous infusion of fucoidin in endotoxin-treated rabbits did not inhibit platelet sequestration in pulmonary capillaries. Conclusion: We conclude that platelets accumulate in alveolar capillaries following endotoxemia. P-selectin expressed on the surface of platelets seems to play an important role in mediating this platelet-endothelial cell interaction. Copyright (c) 2006 S. Karger AG, Basel

The influence of an intense laser beam interaction with preformed plasma on the characteristics of emitted ion streams

AbstractIntense laser-beam interactions with preformed plasma, preceding the laser-target interactions, significantly influence both the ion and X-ray generation. It is due to the laser pulse (its total length, the shape of the front edge, its background, the contrast, the radial homogeneity) as well as plasma (density, temperature) properties. Generation of the super fast (FF) ion groups is connected with a presence of non-linear processes. Saturated maximum of the charge states (independently on the laser intensity) is ascribed to the constant limit radius of the self-focused laser beam. Its longitudinal structure is considered as a possible explanation for the course of some experimental dependencies obtained

A molecular map of murine lymph node blood vascular endothelium at single cell resolution

Blood vascular endothelial cells (BECs) control the immune response by regulating blood flow and immune cell recruitment in lymphoid tissues. However, the diversity of BEC and their origins during immune angiogenesis remain unclear. Here we profile transcriptomes of BEC from peripheral lymph nodes and map phenotypes to the vasculature. We identify multiple subsets, including a medullary venous population whose gene signature predicts a selective role in myeloid cell (vs lymphocyte) recruitment to the medulla, confirmed by videomicroscopy. We define five capillary subsets, including a capillary resident precursor (CRP) that displays stem cell and migratory gene signatures, and contributes to homeostatic BEC turnover and to neogenesis of high endothelium after immunization. Cell alignments show retention of developmental programs along trajectories from CRP to mature venous and arterial populations. Our single cell atlas provides a molecular roadmap of the lymph node blood vasculature and defines subset specialization for leukocyte recruitment and vascular homeostasis

Recent results of studies of magnetic field distribution and neutron scaling on PF-1000 and PF-3 facilities

The recent results of studies of the magnetic field distribution and the neutron yield scaling in two largest plasma focus facilities, PF-3 and PF-1000 is done. The power-law dependence of the neutron yield on the current in the imploding plasma sheath has been demonstrated experimentally. For the first time the presence of the Вz magnetic field components is experimentally shown. In the compression stage, the axial component of the magnetic field reaches several kG that comprises ~10 % of the azimuthal component. The presence of the Bz field is a powerful argument in favor of the existence of closed magnetic configurations, which play an important role in the generating of neutrons.Представлены результаты последних исследований распределения магнитного поля и скейлинга нейтронного выхода на двух крупнейших плазмофокусных установках ПФ-3 и ПФ-1000. Экспериментально показана степенная зависимость нейтронного выхода от величины тока в сжимающейся плазменной оболочке. Впервые экспериментально показано наличие Вz-компоненты магнитного поля. В стадии сжатия величина аксиальной компоненты магнитного поля достигает нескольких килограмм-сил, что составляет ~ 10% от величины азимутальной компоненты. Наличие Bz-поля является весомым аргументом в пользу существования замкнутых магнитных конфигураций, играющих важную роль в механизме генерации нейтронов.Представлено результати останніх досліджень розподілу магнітного поля і скейлінга нейтронного вихoдy на двох найбільших плазмофокусних установках ПФ-3 та ПФ-1000. Експериментально показана ступенева залежність нейтронного виходу від величини струму в плазмовїй оболонці, що стикається. Вперше експериментально показано наявність Вz-компоненти магнітного поля. У стадії стиснення величина аксіальної компоненти магнітного поля досягає декількох кілограм-сил, що складає ~ 10 % від величини азимутальної компоненти. Наявність Вz-поля є вагомим аргументом на користь існування замкнутих магнітних конфігурацій, що мають неаби яку роль у механізмі генерації нейтронів

Neutrophil mobilization via plerixafor-mediated CXCR4 inhibition arises from lung demargination and blockade of neutrophil homing to the bone marrow

Blood neutrophil homeostasis is essential for successful host defense against invading pathogens. Circulating neutrophil counts are positively regulated by CXCR2 signaling and negatively regulated by the CXCR4-CXCL12 axis. In particular, G-CSF, a known CXCR2 signaler, and plerixafor, a CXCR4 antagonist, have both been shown to correct neutropenia in human patients. G-CSF directly induces neutrophil mobilization from the bone marrow (BM) into the blood, but the mechanisms underlying plerixafor-induced neutrophilia remain poorly defined. Using a combination of intravital multiphoton microscopy, genetically modified mice and novel in vivo homing assays, we demonstrate that G-CSF and plerixafor work through distinct mechanisms. In contrast to G-CSF, CXCR4 inhibition via plerixafor does not result in neutrophil mobilization from the BM. Instead, plerixafor augments the frequency of circulating neutrophils through their release from the marginated pool present in the lung, while simultaneously preventing neutrophil return to the BM. Our study demonstrates for the first time that drastic changes in blood neutrophils can originate from alternative reservoirs other than the BM, while implicating a role for CXCR4-CXCL12 interactions in regulating lung neutrophil margination. Collectively, our data provides valuable insights into the fundamental regulation of neutrophil homeostasis, which may lead to the development of improved treatment regimens for neutropenic patients.This research was funded by SIgN, A*STAR, Singapore. C.N.Z. Mattar and J.K.Y. Chan received salary support from the National Medical Research Council of Singapore (NMRC/TA/003/2012 and NMRC/CSA/012/2009, respectively).S

Pichinde virus induces microvascular endothelial cell permeability through the production of nitric oxide

This report is the first to demonstrate infection of human endothelial cells by Pichinde virus (PIC). PIC infection induces an upregulation of the inducible nitric oxide synthase gene; as well as an increase in detectable nitric oxide (NO). PIC induces an increase in permeability in endothelial cell monolayers which can be abrogated at all measured timepoints with the addition of a nitric oxide synthase inhibitor, indicating a role for NO in the alteration of endothelial barrier function. Because NO has shown antiviral activity against some viruses, viral titer was measured after addition of the NO synthase inhibitor and found to have no effect in altering virus load in infected EC. The NO synthase inhibition also has no effect on levels of activated caspases induced by PIC infection. Taken together, these data indicate NO production induced by Pichinde virus infection has a pathogenic effect on endothelial cell monolayer permeability

Candesartan Attenuates Diabetic Retinal Vascular Pathology by Restoring Glyoxalase-I Function

This is an uncopyedited electronic version of an article accepted for publication in Diabetes. The American Diabetes Association, publisher of Diabetes, is not responsible for any errors or omissions in this version of the manuscript or any version derived from it by third parties. The definitive publisher-authenticated version will be available in a future issue of Diabetes in print and online a