No description available.

Case study of a district in Orissa

Co-operatives:Organization and management-policy measures

Thesis (M.A.) - Carleton University, 2009. / Includes bibliographical references (p.55-65). Also available in electronic format on the Internet.

Thesis (M.A.) - Carleton University, 2009. / Includes bibliographical references (p. 107-116). Also available in electronic format on the Internet.

Thesis (Ph. D.)--University OF MICHIGAN.

Thesis (M.S.)--Lehigh University, 2009. / Adviser: Deborah Laible.

Thesis (Ph.D.)--Lehigh University, 2009. / Adviser: Ageliki Nicolopoulou.

<p> What influences the thinking and decision processes of donors when they engage in philanthropy? This study employed developmental psychology to explore this question. Developmental theorists agree that an adult develops in sequential stages over the course of a lifetime, gradually adopting an increasingly complex mental map. An individual&rsquo;s developmental stage at any point in time, theorists argue, is made manifest as a type of &ldquo;action logic&rdquo; through which the individual interprets his/her external world and internal experience. One&rsquo;s action logic is subtle and, for most of one&rsquo;s life, operates outside of conscious awareness. It becomes evident, however, through attitudes, thoughts, and behaviors. In recent years, some theorists have developed techniques to measure an individual&rsquo;s developmental level. </p><p> Stage theories of development have been used successfully for a variety of purposes in a number of fields. To date, however, neither the theory nor the associated measurement techniques have been employed to study philanthropic giving. </p><p> This study, which represents the first step in a long-term research agenda, explored how the action logics of a sample of donors affect philanthropic giving. The purpose was to (1) identify donors&rsquo; action logics, (2) explore what types of influences a donor&rsquo;s action logic may have on a donor&rsquo;s philanthropic decisions; and (3) determine how, if at all, a donor seeks feedback from others or engages in self-reflection regarding his/her philanthropic agenda. </p><p> The study, which included 11 participants, employed a four-phase mixed-methods design. First, qualitative interviews were conducted and data generated were developed into cases studies using a process characterized as narrative analysis. Second, the developmental theory was used to code the data and hypothesize each participant&rsquo;s developmental level(s). Third, three formal tests of trustworthiness were implemented to test the qualitative analysis: member checking of the narrative analysis, triangulation with the results of the Global Leadership Profile instrument, and a formal research audit of three cases. Finally, a cross-case analysis highlighted key themes from the qualitative data.</p>

Neuropilin1 (Npn1) is a transmembrane receptor that is critical for development of both the nervous and vascular systems. It is a ligand for both the chemorepulsive Semaphorin3s and for vascular endothelial growth factor (VEGF), which is a protein critical for proper development, particularly for angiogenesis. Npn1 knockout mice die during early development due to cardiovascular abnormalities, and mice lacking Npn1 in endothelial cells (ECs) die perinatally with similar cardiovascular deficits. Because of the known importance of VEGF in cardiovascular development, it had been thought that the VEGF- Npn1 interaction was responsible for the premature death seen in Npn1 mutants. We identified one amino acid residue (D320) in the b1 domain of Npn1 that is necessary for VEGF-Npn1 binding. By mutating this site, we eliminated VEGF-Npn1 binding in vitro. We then made a knock-in mouse containing the D320K mutation, thus creating a mouse with no VEGF-Npn1 binding \((Npn1^{VEGF-} mouse)\). Surprisingly, the \(Npn1^{VEGF-}\) mutant mouse does not have the premature death or vascular phenotype seen in the Npn1-null. In particular, it does not recapitulate the decreased vascular density or decreased endothelial cell number seen in the Npn1 null. This indicates that the vascular phenotype seen in the Npn1 null is not a result of VEGF-Npn1 binding, and instead implicates that the phenotype is the result of the interaction of Npn1 with its VEGF co-receptor VEGFR2.