3 research outputs found
North Dakota Youth Correctional Center: An Exploration of a Multi-Faceted Campus
The campus of the North Dakota Youth
Correctional Center (NDYCC) lies
nestled between the Heart River to the
east and the scenic buttes to the south.
Just outside the city center of Mandan,
North Dakota. Due to a disconnected
campus, NDYCC is presently struggling
to implement a new treatment entitled,
Educating for Quality by Understanding
Interpersonal Potential (EQUIP), which
is a treatment approach focusing
on cognitive restructuring, anger
management, social skills, and social
decision-making. My project will
address this problem through the
re-design of the campus masterplan
and the design of a new cottage
prototype. To further enable NDYCC?s
treatment theory to reach the next
level of effectiveness, the theoretical
premises of my thesis project will also
focus on the interpersonal potential of
the facility?s occupants, the troubled
adolescents of North Dakota, through
the clear organization and integration
of residence, education, and incentive
programs
Induction of Atrial Fibrillation by Neutrophils Critically Depends on CD11b/CD18 Integrins
Background: Recent observational clinical and ex-vivo studies suggest that inflammation and in particular leukocyte activation predisposes to atrial fibrillation (AF). However, whether local binding and extravasation of leukocytes into atrial myocardium is an essential prerequisite for the initiation and propagation of AF remains elusive. Here we investigated the role of atrial CD11b/CD18 mediated infiltration of polymorphonuclear neutrophils (PMN) for the susceptibility to AF. Methods and Results: C57bl/6J wildtype (WT) and CD11b/CD18 knock-out (CD11b(-/-)) mice were treated for 14 days with subcutaneous infusion of angiotensin II (Ang II), a known stimulus for PMN activation. Atria of Ang II-treated WT mice were characterized by increased PMN infiltration assessed in immunohistochemically stained sections. In contrast, atrial sections of CD11b(-/-) mice lacked a significant increase in PMN infiltration upon Ang II infusion. PMN infiltration was accompanied by profoundly enhanced atrial fibrosis in Ang II treated WT as compared to CD11b(-/-) mice. Upon in-vivo electrophysiological investigation, Ang II treatment significantly elevated the susceptibility for AF in WT mice if compared to vehicle treated animals given an increased number and increased duration of AF episodes. In contrast, animals deficient of CD11b/CD18 were entirely protected from AF induction. Likewise, epicardial activation mapping revealed decreased electrical conduction velocity in atria of Ang II treated WT mice, which was preserved in CD11b(-/-) mice. In addition, atrial PMN infiltration was enhanced in atrial appendage sections of patients with persistent AF as compared to patients without AF. Conclusions: The current data critically link CD11b-integrin mediated atrial PMN infiltration to the formation of fibrosis, which promotes the initiation and propagation of AF. These findings not only reveal a mechanistic role of leukocytes in AF but also point towards a potential novel avenue of treatment in AF