103,114 research outputs found
Meeting and Working with H.T. Engelhardt Jr.: An Inspiring Experience for a (once young) European Scholar
No full textThe author – a European “companion” of H. T. Engelhardt during the two last decades of the 20th century – describes his meetings with and impressions of Tris Engelhardt. He clarifies how open mindedness was the main concern in their common activities
Are language production problems apparent in adults who no longer meet diagnostic criteria for attention-deficit/hyperactivity disorder?
No full textIn this study, we examined sentence production in a sample of adults (N = 21) who had had attention-deficit/hyperactivity disorder (ADHD) as children, but as adults no longer met DSM-IV diagnostic criteria (APA, 2000). This “remitted” group was assessed on a sentence production task. On each trial, participants saw two objects and a verb. Their task was to construct a sentence using the objects as arguments of the verb. Results showed more ungrammatical and disfluent utterances with one particular type of verb (i.e., participle). In a second set of analyses, we compared the remitted group to both control participants and a “persistent” group, who had ADHD as children and as adults. Results showed that remitters were more likely to produce ungrammatical utterances and to make repair disfluencies compared to controls, and they patterned more similarly to ADHD participants. Conclusions focus on language output in remitted ADHD, and the role of executive functions in language production
T-cell trafficking in the central nervous system
No full textTo perform their distinct effector functions, pathogen-specific T cells have to migrate to target tissue where they recognize antigens and produce cytokines that elicit appropriate types of protective responses. Similarly, migration of pathogenic self-reactive T cells to target organs is an essential step required for tissue-specific autoimmunity. In this article, we review data from our laboratory as well as other laboratories that have established that effector function and migratory capacity are coordinately regulated in different T-cell subsets. We then describe how pathogenic T cells can enter into intact or inflamed central nervous system (CNS) to cause experimental autoimmune encephalomyelitis or multiple sclerosis. In particular, we elaborate on the role of CCR6/CCL20 axis in migration through the choroid plexus and the involvement of this pathway in immune surveillance of and autoimmunity in the CNS
Émile-G. Léonard, Le « liber Amicorum » du Strasbourgeois Nicolas Engelhardt (1573-1612). Bibliothèque de l'École des Chartes, t. XCVI, 1935
No full textStrohl Henri. Émile-G. Léonard, Le « liber Amicorum » du Strasbourgeois Nicolas Engelhardt (1573-1612). Bibliothèque de l'École des Chartes, t. XCVI, 1935. In: Revue d'histoire et de philosophie religieuses, 15e année n°6, Novembre-décembre 1935. p. 560
Émile-G. Léonard, Le « liber Amicorum » du Strasbourgeois Nicolas Engelhardt (1573-1612). Bibliothèque de l'École des Chartes, t. XCVI, 1935
No full textStrohl Henri. Émile-G. Léonard, Le « liber Amicorum » du Strasbourgeois Nicolas Engelhardt (1573-1612). Bibliothèque de l'École des Chartes, t. XCVI, 1935. In: Revue d'histoire et de philosophie religieuses, 15e année n°6, Novembre-décembre 1935. p. 560
Helmut Willke: Systemtheorie der Wissensgesellschaft
No full textStrulik T. Helmut Willke: Systemtheorie der Wissensgesellschaft. In: Engelhardt A, Kajetztke L, eds. Handbuch Wissensgesellschaft. Theorien, Themen und Probleme. Bielefeld: transcript; 2010: 65-76
Letter, [Author unclear] to Paulina T. Merritt
No full textHandwritten letter to Paulina Merritt from an unknown author, October 1, 1876.
1913 - The Missions and Missionaries of California, Vol. III, Upper California, Part II, General History, Zephyrin Engelhardt
No full textVolume III, Section I of Engelhardt\u27s series on California missions covers largely the period of 1812 through 1830 addressing the challenges and difficulties facing the missionaries including the scarcity of resources and labor. He described the invasion of Monterey and other ports in Upper California by Hipólte Bouchard in 1818. Section II covers the period of 1830 through 1836 and the secularization of the missions by the Mexican government during which time the missionaries held their posts until either death or the government relieved them of the responsibility of protecting the neophytes against white rapacity and the destruction of the missionary establishments. Engelhardt noted that to secularize an Indian mission, as decreed and practiced under Spanish rule, meant that all the property, save the church building, the priest\u27s habitation, the garden, and the vineyard, should be turned over to the neophytes to be managed in common by officials chosen from among the same neophytes. According to the author, the Californians\u27 greed and disregard for religion were the real motivation behind secularization. Engelhardt discussed in detail Eceandia\u27s Decree of Mission Confiscation issued in 1831, the adverse impact of the Californians on the missions, missionaries and neophytes and efforts to emancipate the Indians. According to Engelhardt, [t]he mission despoilers and their abettors chose to call it \u27secularizaton,\u27 but it was nothing less than brutal confiscation which resulted in the annihilation or dispersion of the Indian converts.https://digitalcommons.csumb.edu/hornbeck_spa_2/1009/thumbnail.jp
Molecular mechanisms involved in T cell migration across the blood-brain barrier
No full textIn the healthy individuum lymphocyte traffic into the central nervous system (CNS) is very low and tightly controlled by the highly specialized blood-brain barrier (BBB). In contrast, under inflammatory conditions of the CNS such as in multiple sclerosis or in its animal model experimental autoimmune encephalomyelitis (EAE) circulating lymphocytes and monocytes/macrophages readily cross the BBB and gain access to the CNS leading to edema, inflammation and demyelination. Interaction of circulating leukocytes with the endothelium of the blood-spinal cord and blood-brain barrier therefore is a critical step in the pathogenesis of inflammatory diseases of the CNS. Leukocyte/endothelial interactions are mediated by adhesion molecules and chemokines and their respective chemokine receptors. We have developed a novel spinal cord window preparation, which enables us to directly visualize CNS white matter microcirculation by intravital fluorescence videomicroscopy. Applying this technique of intravital fluorescence videomicroscopy we could provide direct in vivo evidence that encephalitogenic T cell blasts interact with the spinal cord white matter microvasculature without rolling and that alpha4-integrin mediates the G-protein independent capture and subsequently the G-protein dependent adhesion strengthening of T cell blasts to microvascular VCAM-1. LFA-1 was found to neither mediate the G-protein independent capture nor the G- protein dependent initial adhesion strengthening of encephalitogenic T cell blasts within spinal cord microvessel, but was rather involved in T cell extravasation across the vascular wall into the spinal cord parenchyme. Our observation that G-protein mediated signalling is required to promote adhesion strengthening of encephalitogenic T cells on BBB endothelium in vivo suggested the involvement of chemokines in this process. We found functional expression of the lymphoid chemokines CCL19/ELC and CCL21/SLC in CNS venules surrounded by inflammatory cells in brain and spinal cord sections of mice afflicted with EAE suggesting that the lymphoid chemokines CCL19 and CCL21 besides regulating lymphocyte homing to secondary lymphoid tissue might be involved in T lymphocyte migration into the immuneprivileged CNS during immunosurveillance and chronic inflammation. Here, I summarize our current knowledge on the sequence of traffic signals involved in T lymphocyte recruitment across the healthy and inflamed blood-brain and blood-spinal cord barrier based on our in vitro and in vivo investigations
Preclinical testing of strategies for therapeutic targeting of human T-cell trafficking in vivo
No full textNaive T cells are migratory cells that continuously recirculate between blood and lymphoid tissues. Antigen-specific stimulation of T cells within the lymph nodes reprograms the trafficking properties of T cells by inducing a specific set of adhesion molecules and chemokine receptors on their surface which allow these activated and effector T cells to effectively and specifically home to extralymphoid organs. The observations of organ-specific homing of T cells initiated the development of therapeutic strategies targeting adhesion receptors for organ-specific inhibition of chronic inflammation. As most adhesion receptors have additional immune functions besides mediating leukocyte trafficking, these drugs may have additional immunomodulatory effects. Therapeutic targeting of T-cell trafficking to the central nervous system is the underlying concept of a novel treatment of relapsing remitting multiple sclerosis with the humanized anti-alpha-4-integrin antibody natalizumab. In this chapter, we describe a possible preclinical in vivo approach to directly visualize the therapeutic efficacy of a given drug in inhibiting T-cell homing to a certain organ at the example of the potential of natalizumab to inhibit the trafficking of human T cells to the inflamed central nervous system in an animal model of multiple sclerosis
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