Morphologic predictors of aortic expansion in chronic type B aortic dissection.

AIM To identify morphologic factors affecting aortic expansion in patients with uncomplicated type B aortic dissections. METHODS Computed tomography data of 24 patients (18 male; median age: 61 years), diagnosed with acute uncomplicated type B aortic dissections between 2002 and 2013, were retrospectively reviewed. All patients had at least two computed tomography angiography scans and six months of uneventful follow-up. Computed tomography scans were assessed by two independent readers with regard to presence and number of entry tears. Thoracic and abdominal aortic diameters were derived using image processing software. RESULTS Twenty-two of 24 patients showed aortic expansion over a median computed tomography angiographic follow-up of 33.2 months. Annual rates showed an increase of 1.7 mm for total aortic diameter, 2.1 mm for the false and a decrease of -0.4 mm for the true lumen. In three patients (12.5%), aortic diameter exceeded 60 mm during follow-up, and all three patients underwent thoracic endovascular aortic repair. Patients with a maximum aortic diameter <4 cm at baseline showed a significantly higher expansion rate compared to cases with an initial maximum aortic diameter of ≥4 cm (p=0.0471). A median of two entries (range: 1-5) was recognized per patient. Presence of more than two entry tears (n = 13) was associated with faster overall diameter expansion (mean annual rates: 2.18 mm vs. 1.16 mm; p = 0.4556), and decrease of the cross-sectional surface of the true lumen over time (annual rate for > 2 entries vs. ≤2 entries: -7.8 mm(2) vs. +37.5 mm(2); p = 0.0369). Median size of entry tears was 12 mm (range: 2-53 mm). CONCLUSIONS The results presented herein suggest that uncomplicated type B aortic dissection patients with more than two entry tears and/or an initial maximum aortic diameter of<4 cm are at risk for aortic dilatation and, therefore, may require stricter follow-up including the possible need for early intervention.

Expansion load: recessive mutations and the role of standing genetic variation

Expanding populations incur a mutation burden – the so-called expansion load. Previous studies of expansion load have focused on codominant mutations. An important consequence of this assumption is that expansion load stems exclusively from the accumulation of new mutations occurring in individuals living at the wave front. Using individual-based simulations, we study here the dynamics of standing genetic variation at the front of expansions, and its consequences on mean fitness if mutations are recessive. We find that deleterious genetic diversity is quickly lost at the front of the expansion, but the loss of deleterious mutations at some loci is compensated by an increase of their frequencies at other loci. The frequency of deleterious homozygotes therefore increases along the expansion axis, whereas the average number of deleterious mutations per individual remains nearly constant across the species range. This reveals two important differences to codominant models: (i) mean fitness at the front of the expansion drops much faster if mutations are recessive, and (ii) mutation load can increase during the expansion even if the total number of deleterious mutations per individual remains constant. We use our model to make predictions about the shape of the site frequency spectrum at the front of range expansion, and about correlations between heterozygosity and fitness in different parts of the species range. Importantly, these predictions provide opportunities to empirically validate our theoretical results. We discuss our findings in the light of recent results on the distribution of deleterious genetic variation across human populations and link them to empirical results on the correlation of heterozygosity and fitness found in many natural range expansions.

Blocking of LFA-1 enhances expansion of Th17 cells induced by human CD14(+) CD16(++) nonclassical monocytes.

Among human peripheral blood (PB) monocyte (Mo) subsets, the classical CD14(++) CD16(-) (cMo) and intermediate CD14(++) CD16(+) (iMo) Mos are known to activate pathogenic Th17 responses, whereas the impact of nonclassical CD14(+) CD16(++) Mo (nMo) on T-cell activation has been largely neglected. The aim of this study was to obtain new mechanistic insights on the capacity of Mo subsets from healthy donors (HDs) to activate IL-17(+) T-cell responses in vitro, and assess whether this function was maintained or lost in states of chronic inflammation. When cocultured with autologous CD4(+) T cells in the absence of TLR-2/NOD2 agonists, PB nMos from HDs were more efficient stimulators of IL-17-producing T cells, as compared to cMo. These results could not be explained by differences in Mo lifespan and cytokine profiles. Notably, however, the blocking of LFA-1/ICAM-1 interaction resulted in a significant increase in the percentage of IL-17(+) T cells expanded in nMo/T-cell cocultures. As compared to HD, PB Mo subsets of patients with rheumatoid arthritis were hampered in their T-cell stimulatory capacity. Our new insights highlight the role of Mo subsets in modulating inflammatory T-cell responses and suggest that nMo could become a critical therapeutic target against IL-17-mediated inflammatory diseases.

Control of Vertical Dimension During Rapid Palatal Expansion Using a High Pull Chin

Submitted in partial fulfillment of the requirements for a Certificate in Orthodontics, Dept. of Orthodontics, University of Connecticut Health Center, 1986

Stability of Rapid Maxillary Expansion

Submitted in partial fulfillment of the requirements for a Certificate in Orthodontics, Dept. of Orthodontics, University of Connecticut Health Center, 1993

Na 50 Nachlass Arthur Schopenhauer - 'Schopenhauer-Archiv', 432 - Stichworte zu Kant, Schelling, Jacobi und Fries

4 Seiten

Jacobi Rhenferdii ... dissertationes philologicae de Decem Otiosis Synagogae : in quibus viri clariss. Johannis Lightfooti, aliorum que sententiae de Otiosis examinatur, varia de Synagogis, earumque jure, praefectis, ministris ... adsperguntur

Univ., Diss., 1686

F. W. J. Schelling's Denkmal der Schrift von den göttlichen Dingen &c. des Herrn Friedrich Heinrich Jacobi und der ihm in derselben gemachten Beschuldigung eines absichtlich täuschenden, Lüge redenden Atheismus

Denkmal der Schrift von den göttlichen Dingen & des Herrn Friedrich Heinrich Jacobi und der ihm in derselben gemachten Beschuldigung eines absichtlich täuschenden, Lüge redenden Atheismus

Bernhard von Jacobi als Dorantes, Rollenbild, Kniestück, in: Pierre Carlet de Marivaux: Das Spiel von Liebe und Zufall

Signatur des Originals: S 36/F04765

Bernhard von Jacobi als Dorantes, Rollenbild, in: Pierre Carlet de Marivaux: Das Spiel von Liebe und Zufall

Signatur des Originals: S 36/F04766

Bernhard von Jacobi als Tod, Rollenbild

Signatur des Originals: S 36/F04767

Na 1 Nachlass Max Horkheimer, 694 - "German Economy, Politics and Culture, 1900-1933", "The Collapse of German Democracy and the Expansion of National Socialism" (p. IX 168e - IX 169a)

"German Economy, Politics and Culture, 1900-1933. A Research Project of the International Institute of Social Research" (1940):; 1. Umriß des Forschungsprojekts: e)-g) Fassung vom 25.5.1940: e) Typoskript, 63 Blatt, f) Typoskript mit handschriftlichen Korrekturen, 61 Blatt, g) Typoskript, 61 Blatt, h)-k) "Introduction": h) Typoskript, 21 Blatt, i) Typoskript, 15 Blatt, k) D.V. Glass: Entwurf, Manuskript, 17 Blatt; 2. Kostenschätzung zum Forschungsprojekt. 1 Blatt; "The Collapse of German Democracy and the Expansion of National Socialism" (1940):; 1. Darstellung des Forschungsprojekts (15.9.1940), a) als Typoskript vervielfältigt, 70 Blatt;