20 research outputs found
The Gallery 2011
This is a digital copy of the print content produced by the Gallery 2011 team. The Gallery 2011 consists of a box containing a leaflet, four books, and a USB drive. The leaflet lists the works contained on the USB drive in the areas of Time Based Media and Web Design, and provides credits for the Gallery design production team. Content from the USB drive is not included.
The four books contain the artistic works of students in the following genres: Core Studio/Painting, Graphic Design/Illustration, Photography/Printmaking, and Jewelry & Metals/Three Dimensional. Files for individual sections may be viewed on the detailed metadata page by clicking on the book title.https://rdw.rowan.edu/the_gallery/1005/thumbnail.jp
A compact and cost-effective hard X-ray free-electron laser driven by a high-brightness and low-energy electron beam
We present the first lasing results of SwissFEL, a hard X-ray free-electron laser (FEL) that recently came into operation at the Paul Scherrer Institute in Switzerland. SwissFEL is a very stable, compact and cost-effective X-ray FEL facility driven by a low-energy and ultra-low-emittance electron beam travelling through short-period undulators. It delivers stable hard X-ray FEL radiation at 1-Ă… wavelength with pulse energies of more than 500 ÎĽJ, pulse durations of ~30 fs (root mean square) and spectral bandwidth below the per-mil level. Using special configurations, we have produced pulses shorter than 1 fs and, in a different set-up, broadband radiation with an unprecedented bandwidth of ~2%. The extremely small emittance demonstrated at SwissFEL paves the way for even more compact and affordable hard X-ray FELs, potentially boosting the number of facilities worldwide and thereby expanding the population of the scientific community that has access to X-ray FEL radiation
Entwicklung einer Methode zur Untersuchung der biomechanischen Eigenschaften der endothelialen Oberflächensicht
Introduction: We have recently found in isolated human umbilical vein
endothelial cells (HUVEC) that turbulent (atheroprone) vascular shear stress
(VSS) down regulates endothelial connexin 40 and up regulates C6- and V1-type
transient receptor potential (TRP) channels. However the mechanism for these
atheroprone changes is poorly understood. We have shown that atheroprone VSS
profile down regulates the synthesis of a major component of the endothelial
surface layer (ESL), hyaluronan (HA). These findings together with the
extensive amount of publications showing the importance of ESL in endothelial
VSS sensation led us to speculate, that HA might be part of an atheroprone
circulus vitiosus: in the absence of atheroprotective VSS, HA expression
decreases. This leads to decrease of vascular VSS sensitivity followed by
further reduction of HA expression. Thus we aimed at developing a tool to
probe the properties and thickness of the surface layer of cultured HUVECs to
allow investigation the role of HA for VSS related alterations of the ESL.
Methods: A defocus imaging based single particle tracking application was
developed. It allows tracking the 3D position of fluorescent nanobeads with a
precision beyond the diffraction resolution limit. Local viscosity can be
assessed by quantifying the nanobeads’ Brownian motion. Results and
conclusion: For a vertical range of 4.5 µm, the validity of vertical single
particle tracking was 16 nm, with a precision of about 5 nm. In the horizontal
plane precision was 5 nm. In first experiments with HUVEC we could show an
increase of local viscosity in a region close to the cell surface with a
thickness of about 1000 nm which may correspond to the ESL. Thus, the
established approach has the potential to study biophysical properties of the
ESL, including thickness and viscosity. This should allow to investigate the
alteration of ESL beside different pathological conditions.EinfĂĽhrung: In vorhergehenden Untersuchungen konnten wir zeigen, dass in
isolierten Endothelzellen aus humanen Nabelschnurvenen (HUVEC) durch pulsatile
Wandschubspannung bei unidirektionaler laminarer Strömung („atheroprotective
flow profile“) die Expression von Konnexin40 und HAS2 induziert wird. Dagegen
wird die Expression von TNFα sowie C6- und V1-Transient Rezeptor Potential
(TRP) Ionkanälen bei relativ niedriger, oszillierender Wandschubspannung
(atherogenes Strömungsprofil) induziert. Wir konnten auch zeigen, dass durch
ein atherogenes Strömungsprofil die Synthese der wichtigsten Komponente der
endothelialen Oberflächenschicht (ESL), der Hyaluronsäure (HA) unterdrückt
wird. In Verbindung mit der umfangreichen Literatur ĂĽber die Bedeutung des ESL
fĂĽr die Schubspannungsempfindlichkeit von Endothelzellen fĂĽhren diese
Ergebnisse zu der Vermutung, dass die ESL eine zentrale Rolle in einem
proatherogenen circulus vitiosus spielen könnte: durch atherogene
Strömungsbedingungen wird die HA-Synthese reduziert, dies führt zur Reduktion
der ESL Dicke und der Schubspannungs-Empfindlichkeit des Endothels und damit
zur weiterer Unterdrückung der Hyaluronsäureexpression. Um diese Hypothese
testen zu können und die Rolle von Hyaluronsäure und Schubspannung für
Veränderungen der ESL zu überprüfen, wurde eine Methode zur direkte Messung
der Eigenschaften und Dicke der ESL von primären kultivierten Endothelzelle
entwickelt. Methoden: Die Dicke der ESL beträgt ca. 0.5-1 µm und erfordert
damit Messverfahren unterhalb der Auflösungsgrenze des Lichtmikrokops. Dies
wurde durch Bestimmung des Durchmessers von Beugungsringen fluoreszierender
Nanopartikel auĂźerhalb der Fokusebene erreicht. Zur off-line Auswertung
entsprechender mikroskopischer Aufnahmen erfolgte mit einem eigenen Programm
zum automatisierten Einzelpartikel-Tracking. Neben der Bestimmung der Position
des jeweiliges Partikels in den drei Raumachsen war so zugleich die Messung
der Viskosität des umgebenden Mediums möglich. Ergebnisse und Zusammenfassung:
Über einen vertikalen Bereich von 4,5 µm betrug die Validität für die
Lokalisation einzelner Nanopartikel in der Senkrechten 16 nm bei einer
Präzision von etwa 5 nm in der Vertikalen und 5 nm in der Horizontalen. In
ersten Experimenten mit HUVECs, konnten wir einen Anstieg der Viskosität in
Bereichen nahe der Zelloberfläche mit einer Schichtdicke von etwa 1000nm
zeigen. Dieser Bereich könnte der endothelialen Oberflächenschicht
entsprechen. Somit hat das entwickelte Verfahren das Potential, die
biophysikalischen Eigenschaften der ESL, besonders Viskosität und Dicke, zu
untersuchen. Damit können die wandschubspannungs-bedingten frühen Effekte der
endothelialen Dysfunktion, insbesondere die Bedeutung der ESL und der
Hyaluronsäure, weiter untersucht werden
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Role of the endothelial surface layer in neutrophil recruitment.
Neutrophil recruitment in most tissues is limited to postcapillary venules, where E- and P-selectins are inducibly expressed by venular endothelial cells. These molecules support neutrophil rolling via binding of PSGL-1 and other ligands on neutrophils. Selectins extend ≤ 38 nm above the endothelial plasma membrane, and PSGL-1 extends to 50 nm above the neutrophil plasma membrane. However, endothelial cells are covered with an ESL composed of glycosaminoglycans that is ≥ 500 nm thick and has measurable resistance against compression. The neutrophil surface is also covered with a surface layer. These surface layers would be expected to completely shield adhesion molecules; thus, neutrophils should not be able to roll and adhere. However, in the cremaster muscle and in many other models investigated using intravital microscopy, neutrophils clearly roll, and their rolling is easily and quickly induced. This conundrum was thought to be resolved by the observation that the induction of selectins is accompanied by ESL shedding; however, ESL shedding only partially reduces the ESL thickness (to 200 nm) and thus is insufficient to expose adhesion molecules. In addition to its antiadhesive functions, the ESL also presents neutrophil arrest-inducing chemokines. ESL heparan sulfate can also bind L-selectin expressed by the neutrophils, which contributes to rolling and arrest. We conclude that ESL has both proadhesive and antiadhesive functions. However, most previous studies considered either only the proadhesive or only the antiadhesive effects of the ESL. An integrated model for the role of the ESL in neutrophil rolling, arrest, and transmigration is needed
Role of the endothelial surface layer in neutrophil recruitment.
Neutrophil recruitment in most tissues is limited to postcapillary venules, where E- and P-selectins are inducibly expressed by venular endothelial cells. These molecules support neutrophil rolling via binding of PSGL-1 and other ligands on neutrophils. Selectins extend ≤ 38 nm above the endothelial plasma membrane, and PSGL-1 extends to 50 nm above the neutrophil plasma membrane. However, endothelial cells are covered with an ESL composed of glycosaminoglycans that is ≥ 500 nm thick and has measurable resistance against compression. The neutrophil surface is also covered with a surface layer. These surface layers would be expected to completely shield adhesion molecules; thus, neutrophils should not be able to roll and adhere. However, in the cremaster muscle and in many other models investigated using intravital microscopy, neutrophils clearly roll, and their rolling is easily and quickly induced. This conundrum was thought to be resolved by the observation that the induction of selectins is accompanied by ESL shedding; however, ESL shedding only partially reduces the ESL thickness (to 200 nm) and thus is insufficient to expose adhesion molecules. In addition to its antiadhesive functions, the ESL also presents neutrophil arrest-inducing chemokines. ESL heparan sulfate can also bind L-selectin expressed by the neutrophils, which contributes to rolling and arrest. We conclude that ESL has both proadhesive and antiadhesive functions. However, most previous studies considered either only the proadhesive or only the antiadhesive effects of the ESL. An integrated model for the role of the ESL in neutrophil rolling, arrest, and transmigration is needed
Effector and Regulatory T Cells Roll at High Shear Stress by Inducible Tether and Sling Formation
The adaptive immune response involves T cell differentiation and migration to sites of inflammation. T cell trafficking is initiated by rolling on inflamed endothelium. Tethers and slings, discovered in neutrophils, facilitate cell rolling at high shear stress. Here, we demonstrate that the ability to form tethers and slings during rolling is highly inducible in T helper 1 (Th1), Th17, and regulatory T (Treg) cells but less in Th2 cells. In vivo, endogenous Treg cells rolled stably in cremaster venules at physiological shear stress. Quantitative dynamic footprinting nanoscopy of Th1, Th17, and Treg cells uncovered the formation of multiple tethers per cell. Human Th1 cells also showed tethers and slings. RNA sequencing (RNA-seq) revealed the induction of cell migration and cytoskeletal genes in sling-forming cells. We conclude that differentiated CD4 T cells stabilize rolling by inducible tether and sling formation. These phenotypic changes approximate the adhesion phenotype of neutrophils and support CD4 T cell access to sites of inflammation
Neutrophil recruitment limited by high-affinity bent β2 integrin binding ligand in cis.
Neutrophils are essential for innate immunity and inflammation and many neutrophil functions are β2 integrin-dependent. Integrins can extend (E(+)) and acquire a high-affinity conformation with an 'open' headpiece (H(+)). The canonical switchblade model of integrin activation proposes that the E(+) conformation precedes H(+), and the two are believed to be structurally linked. Here we show, using high-resolution quantitative dynamic footprinting (qDF) microscopy combined with a homogenous conformation-reporter binding assay in a microfluidic device, that a substantial fraction of β2 integrins on human neutrophils acquire an unexpected E(-)H(+) conformation. E(-)H(+) β2 integrins bind intercellular adhesion molecules (ICAMs) in cis, which inhibits leukocyte adhesion in vitro and in vivo. This endogenous anti-inflammatory mechanism inhibits neutrophil aggregation, accumulation and inflammation