9,443 research outputs found
Festschrift Heinrich Müller-Breslau /
No full text-- Der starre elastisch gestützte Körper und seine Anwendung bei der geometrischen Behandlung mehrfach statisch unbestimmter Systeme / R. Skutsch.Includes bibliographical references.Ingenieur-Aufgaben / H. Boost -- Über den Windverband versteifter Hängebrücken / O. Domke -- Mitteilung über die Existenzbedingungen von reziproken Kräfteplänen ebener einfacher Fachwerke / M. Grübler -- Die Lösung linearer Gleichungen durch unendliche Reihen und ihre Anwendung auf die Berechnung hochgradig unbestimmter Systeme / A. Hertwig -- Über die Möglichkeit, n-punkte in der Ebene oder im Raume durch weniger als 2 n--3 oder 3 n--6 Stäbe von ganz unveränderlicher Länge unverschieblich miteinander zu verbinden / E. Kötter -- Über das Gleichgewicht elastischer Platten und langer Streifen / F. Kötter -- Zusatzspannungen infolge starrer Knotenverbindung / Th. Landsberg -- Das strebenlose Ständerfachwerk / L. Mann -- Zur Theorie statisch unbestimmter, hölzerner Dachbinder des Hochbaues / S. Müller -- Spannungen in Kugelschalen (Kuppeln) / H. ReissnerMode of access: Internet
Il poeta come "centrifuga di metafore". Heiner Müller sul declino dell'Impero.
No full text"Il poeta come ‘centrifuga di metafore’” fa parte della famosa serie di interviste di Alexander Kluge a Heiner Müller. Si tratta di una vera e propria messa in scena di un dialogo in cui Müller riflette su ciò che viene dimenticato dalla storia e sulle possibilità di rappresentarlo a teatro.
La messa in scena è visibile anche nella forma stessa dell’intervista, che è tutta intessuta di didascalie che descrivono la scena in cui si svolge il dialogo
A Mosaic of Words and Images. Translation and Commentary of Herta Müller's "Der Beamte sagte".
No full textreservedDie vorliegende Arbeit bietet einen Übersetzungsvorschlag vom Deutschen ins Italienische des Buchs Der Beamte sagte der rumäniendeutschen Schriftstellerin Herta Müller. Hauptziel dieser Arbeit ist es, bestimmte Übersetzungsschwierigkeiten hervorzuheben und über die entsprechenden Lösungen zu überlegen. Insbesondere werden die Übersetzungsentscheidungen von für den Text prägenden Stilelementen, beispielweise Metaphern, gründlich untersucht. Die Übersetzung des Textes und ihren Kommentar zeigen also die Komplexität von Müllers hochpoetischer Sprache und die Herausforderungen, die sie an den Übersetzer stellt.The following is a translation draft from German into Italian of the book Der Beamte sagte by the Romanian-German author Herta Müller. The main aim of this work is to highlight some problems of translation and focus on any possible solutions. Particularly, translation choices of certain stylistic elements characterizing the book of Müller, such as metaphors, are shown. The translation of the text and its commentary thus reveal the complexity of Müller’s highly poetic language and the challenges for the translator
Müller Deutschland 1979-1989. L'istituzione Heiner Müller nella Repubblica Federale Tedesca attraverso l'esempio di Berlino Ovest
No full textObject of this essay is role of the GDR author and dramatist Heiner Müller in West Berlin between 1979 and 1989, contextualizing him in the specific and peculiar artistic and intellectual scenario of the so called "two hearted city"
Vegf‐independent activation of müller cells by the vitreous from proliferative diabetic retinopathy patients
No full textProliferative diabetic retinopathy (PDR), a major complication of diabetes mellitus, results from an inflammation‐sustained interplay among endothelial cells, neurons, and glia. Even though anti‐vascular endothelial growth factor (VEGF) interventions represent the therapeutic option for PDR, they are only partially efficacious. In PDR, Müller cells undergo reactive gliosis, produce inflammatory cytokines/chemokines, and contribute to scar formation and retinal neovascularization. However, the impact of anti‐VEGF interventions on Müller cell activation has not been fully elucidated. Here, we show that treatment of MIO‐M1 Müller cells with vitreous obtained from PDR patients stimulates cell proliferation and motility, and activates various intracellular signaling pathways. This leads to cytokine/chemokine upregulation, a response that was not mimicked by treatment with recombinant VEGF nor inhibited by the anti‐VEGF drug ranibizumab. In contrast, fibroblast growth factor‐2 (FGF2) induced a significant overexpression of various cytokines/chemokines in MIO‐M1 cells. In addition, the FGF receptor tyrosine kinase inhibitor BGJ398, the pan‐FGF trap NSC12, the heparin‐binding protein antagonist N‐tert-butyloxycarbonyl‐Phe‐Leu‐Phe‐Leu‐Phe Boc2, and the anti‐inflammatory hydrocortisone all inhibited Müller cell activation mediated by PDR vitreous. These findings point to a role for various modulators beside VEGF in Müller cell activation and pave the way to the search for novel therapeutic strategies in PDR
Non-solvability for a class of left-invariant second-order differential operators on the Heisenberg group
No full textWe study the question of local solvability for second-order, left-invariant differential operators on the Heisenberg group , of the form
where is a complex matrix. Such operators never satisfy a cone condition in the sense of Sjöstrand and Hörmander. We may assume that cannot be viewed as a differential operator on a lower-dimensional Heisenberg group. Under the mild condition that and their commutator are linearly independent, we show that is not locally solvable, even in the presence of lower-order terms, provided that . In the case we show that there are some operators of the form described above that are locally solvable. This result extends to the Heisenberg group a phenomenon first observed by Karadzhov and Müller in the case of It is interesting to notice that the analysis of the exceptional operators for the case turns out to be more elementary than in the case When the analysis of these operators seems to become quite complex, from a technical point of view, and it remains open at this time
Aqueous Humor Biomarkers of Müller Cell Activation in Diabetic Eyes
No full textPurpose: To identify early biomarkers of retinal Müller cell activation in diabetic eyes with or without clinically detectable signs of diabetic retinopathy (DR).
Methods: This study was a cross-sectional comparative case series. The aqueous humor (AH) of 34 eyes was collected in 12 healthy controls, 11 diabetic patients without DR, and 11 diabetic patients with nonproliferative DR. Full ophthalmic examination and spectral-domain optical coherence tomography were performed in all eyes. Glial fibrillary acidic protein (GFAP), aquaporin 1 (AQP1), and aquaporin 4 (AQP4) were quantified in AH samples as biomarkers of Müller cell activity by ELISA. Statistical analysis was performed with ANOVA followed by Tukey-Kramer post hoc test.
Results: There was no significant difference in the age among the three groups. Mean concentration of GFAP, AQP1, and AQP4 significantly increased in diabetic eyes versus controls (P < 0.05, for each comparison). Glial fibrillary acidic protein and AQP1 showed an approximate 2-fold increase, whereas AQP4 showed an approximate 25-fold increase in diabetics with DR versus controls. In diabetics without DR, AQP4 showed an approximate 6-fold increase versus controls.
Conclusions: Glial fibrillary acidic protein, AQP1, and AQP4-biomarkers of Müller cell activity-are significantly increased in human eyes with diabetes, confirming that Müller cells are precociously affected by diabetes mellitus
Aqueous Humor Biomarkers of Müller Cell Activation in Diabetic Eyes.
No full textPURPOSE:
To identify early biomarkers of retinal Müller cell activation in diabetic eyes with or without clinically detectable signs of diabetic retinopathy (DR).
METHODS:
This study was a cross-sectional comparative case series. The aqueous humor (AH) of 34 eyes was collected in 12 healthy controls, 11 diabetic patients without DR, and 11 diabetic patients with nonproliferative DR. Full ophthalmic examination and spectral-domain optical coherence tomography were performed in all eyes. Glial fibrillary acidic protein (GFAP), aquaporin 1 (AQP1), and aquaporin 4 (AQP4) were quantified in AH samples as biomarkers of Müller cell activity by ELISA. Statistical analysis was performed with ANOVA followed by Tukey-Kramer post hoc test.
RESULTS:
There was no significant difference in the age among the three groups. Mean concentration of GFAP, AQP1, and AQP4 significantly increased in diabetic eyes versus controls (P < 0.05, for each comparison). Glial fibrillary acidic protein and AQP1 showed an approximate 2-fold increase, whereas AQP4 showed an approximate 25-fold increase in diabetics with DR versus controls. In diabetics without DR, AQP4 showed an approximate 6-fold increase versus controls.
CONCLUSIONS:
Glial fibrillary acidic protein, AQP1, and AQP4-biomarkers of Müller cell activity-are significantly increased in human eyes with diabetes, confirming that Müller cells are precociously affected by diabetes mellitus
Self-calibration of RA-PKM via motion reverse points: A procedure based on an analytical indicator function
No full textA novel optimization algorithm for the calibration of redundantly actuated parallel manipulator (RA-PKM) is presented. The method uses an analytical indicator function (IF) which takes a specific value at the motion reversal points (MRP). MRP are configurations where the speed of one passive actuator vanishes during a continuous motion. IF depends on the passive actuator, the locked actuators, the geometrical parameters. The main idea is to perform an optmization that makes the IF equal to the specific value at the MRP whenever the geometrical parameters match the real values. Simulations of the calibration of a planar 4-RPR RA-PKM are presented. Communicated by S. Velinsk
MÜLLER GLIAL CELLS IN EPIRETINAL MEMBRANE FORMATION
No full textUna membrana epiretinica (ERM) è un sottile strato di tessuto fibroso che può formarsi sulla superficie dell'area maculare della retina e causare problemi alla vista.Le cellule gliali di Müller sembrano svolgere un ruolo fondamentale nella patogenesi dell'ERM, dove varie citochine e fattori di crescita possono agire come modulatori autocrini e paracrini innescando la proliferazione, la migrazione, la transdifferenziazione e l'aumento dell'espressione dei marcatori della gliosi delle cellule di Müller. L'umor vitreo può rappresentare un serbatoio di mediatori patologici che si accumu
Durante la prima parte del mio dottorato di ricerca ho partecipato a un progetto in cui abbiamo dimostrato che gli iERM rimossi chirurgicamente sono caratterizzati da un diverso pattern di espressione di geni associati a diverse popolazioni cellulari, matrice extracellulare e biomarcatori di citochine/fattori di crescita rilevanti per la patogenesi della malattia. Inoltre, il raggruppamento gerarchico dei dati di espressione genica ha identificato due cluster molecolari di membrane iERM associati a caratteristiche cliniche e SD-OCT distinte (denominate iERM-A e iERM-B). I pazienti iERM-A sono caratterizzati da manifestazioni cliniche meno gravi e un profilo di espressione genica iERM più "quiescente" rispetto ai pazienti iERM-B.
Inoltre, mi sono concentrato sulla comprensione del ruolo delle cellule gliali di Müller nella patogenesi di iERM. Durante la progressione di iERM, le cellule gliali di Müller subiscono una transizione gliale-mesenchimale (GMT), un processo di transdifferenziazione caratterizzato dalla sottoregolazione dei marcatori delle cellule di Müller parallela alla sovraregolazione dei marcatori dei miofibroblasti pro-fibrotici. Il presente studio ha dimostrato che il fluido vitreo ottenuto dai pazienti iERM induce proliferazione, migrazione e GMT nelle cellule MIO-M1 Müller, un fenotipo coerente con il comportamento delle cellule Müller durante la progressione iERM. Tuttavia, anche se
il fluido vitreo ottenuto dai pazienti iERM-A potrebbe indurre un GMT completo nelle cellule MIO-M1, i campioni iERM-B hanno causato solo un GMT parziale, caratterizzato dalla downregulation dei marker cellulari di Müller in assenza di upregulation di pro- marcatori fibrotici di miofibroblasti.
Per la parte finale del mio lavoro di tesi, ho utilizzato il fluido vitreo ottenuto da pazienti con PDR come strumento per studiare l'attivazione che si verifica nelle cellule di Müller durante la PDR. I risultati mostrano che il vitreo PDR induce l'acquisizione di un fenotipo attivato nelle cellule di Müller, caratterizzato da un aumento della proliferazione e della migrazione cellulare, dall'attivazione del segnale intracellulare e dall'espressione di citochine/chemochine proinfiammatorie. Sorprendentemente, abbiamo scoperto che l'acquisizione di questo fenotipo non è correlata alla stimolazione del VEGF, mentre il trattamento delle cellule di Müller con il fattore di crescita dei fibroblasti di base (FGF2) induce un aumento significativo dell'espressione di varie citochine/chemochine nelle cellule MIO-M1. Di conseguenza, il farmaco anti-VEGF ranibizumab non influenza l'attivazione delle cellule di Müller mediata dal vitreo PDR mentre il trattamento con l'inibitore della tirosin-chinasi del recettore dell'FGF (FGFR) BGJ398, la trappola pan-FGF NSC12, l'antagonista della proteina legante l'eparina multi-target N- tert-butyloxycarbonyl-Phe-Leu-Phe-Leu-Phe Boc2, o il farmaco antinfiammatorio idrocortisone inibisce, almeno in parte, l'attività dei campioni vitrei PDR.
Insieme, i risultati indicano che potrebbe esistere una relazione tra la capacità del vitreo iERM di modulare il GMT nelle cellule di Müller, il profilo molecolare dei corrispondenti iERM e le caratteristiche cliniche dei pazienti iERM. Inoltre, questi dati indicano un ruolo per vari mediatori oltre al VEGF nella risposta suscitata dal vitreo PDR nelle cellule di Müller.An epiretinal membrane (ERM) is a thin layer of fibrous tissue that can form on the surface of the retina macular area and cause vision problems. Müller glial cells appear to play a pivotal role in the pathogenesis of ERM, where various cytokines and growth factors may act as autocrine and paracrine modulators by triggering Müller cell proliferation, migration, collagen contraction, transdifferentiation, and increased expression of gliosis markers. Vitreous humor may represent a reservoir of pathological mediators that accumulate during the progression of retinal diseases. Here, the vitreous fluid obtained from iERM and PDR patients was used as a tool to investigate the activation that occurs in Müller cells in disease progression.
During the first part of my Ph.D. thesis work, I participated in a research project in which we showed that surgically removed iERMs are characterized by a different pattern of expression of a series of the cell population, extracellular matrix, and cytokine/growth factor biomarkers relevant to the pathogenesis of the disease. Further, the hierarchical clustering of the gene expression data identified two molecular clusters of iERM membranes associated with distinct clinical and SD-OCT features (named iERM-A and iERM-B). iERM-A patients are characterized by less severe clinical features and a more "quiescent" iERM gene expression profile when compared to iERM-B patients.
Further, I focused on understanding the role of Müller glial cells in the pathogenesis of iERM. During the progression of iERM, Müller glial cells undergo a glial-to-mesenchymal transition (GMT), a transdifferentiation process characterized by the downregulation of Müller cell markers paralleled by the upregulation of pro-fibrotic myofibroblast markers. The present study demonstrated that the vitreous fluid obtained from the iERM patients induces proliferation, migration, and GMT in MIO-M1 Müller cells, a phenotype consistent with Müller cell behaviour during iERM progression. However, even though the vitreous fluid obtained from iERM-A patients could induce a complete GMT in MIO-M1 cells, iERM-B samples caused only a partial GMT, characterized by the downregulation of Müller cell markers in the absence of upregulation of pro-fibrotic myofibroblast markers.
For the final part of my thesis work, the vitreous fluid obtained from PDR patients was used as a tool to investigate the activation that occurs in Müller cells during PDR. The results show that PDR vitreous induces the acquisition of an activated phenotype in Müller cells, characterized by an increase in cell proliferation and migration, intracellular signalling activation, and proinflammatory cytokine/chemokine expression. Surprisingly, we found that the acquisition of this phenotype is not related to VEGF stimulation, whereas treatment of Müller cells with basic fibroblast growth factor (FGF2) induces a significant increase in the expression of various cytokines/chemokines in MIO-M1 cells. Accordingly, the anti-VEGF drug ranibizumab does not affect Müller cell activation mediated by PDR vitreous whereas treatment with the FGF receptor (FGFR) tyrosine kinase inhibitor BGJ398, the pan-FGF trap NSC12, the multi-target heparin-binding protein antagonist N-tert-butyloxycarbonyl-Phe-Leu-Phe-Leu-Phe Boc2, or the anti-inflammatory drug hydrocortisone inhibits, at least in part,the activity of PDR vitreous samples.
Together, the results indicate that a relationship may exist among the ability of iERM vitreous to modulate GMT in Müller cells, the molecular profile of the corresponding iERMs, and the clinical features of iERM patients. Also, these data point to a role for various mediators besides VEGF in the response elicited by PDR vitreous in Müller cells
- …
