We examine the effects that two accounting measures of nonprofit organization (NPO) inefficiency, administrative inefficiency and donation price, have on donations to US NPOs using a better‐specified model and industry‐specific samples. Although numerous studies examine the effect that donation price has on donations (e.g., Marudas and Jacobs, 2006; Marudas, 2004; Khanna and Sandler, 2000; and Tinkelman, 1999), only three studies examine the effect of administrative inefficiency on donations (Tinkelman and Mankaney, 2007; Frumkin and Kim, 2001; and Greenlee and Brown, 1999). However, none of these studies tests donation price and administrative inefficiency in one model and only two test industry‐specific samples of NPOs. We find that misspecifying the model by including only one of these two inefficiency measures creates substantial bias and the effect of administrative inefficiency on donations varies substantially across industries. Administrative inefficiency has a significantly negative effect on donations to NPOs in the full sample and the philanthropy sample, but no significant effect on donations to NPOs in the arts, education, health, or human services samples. Furthermore, donation price has a significantly negative effect on donations to NPOs in the full sample and the education, health and human services samples, but not in the arts or philanthropy samples. Results are also reported for the other variables in the model – government support, program service revenue, fundraising and organizational age, wealth and size.

Communicated by J.H.Weil tant of Bradyrhizobiumjaponicum, the amounts of GS mRNA did not increase over that in roots. These experiments, together with the time course of increase in GS mRNA transcripts, suggest that the genes encoding cytosolic GS are directly induced by the available ammonia.

Human mucin 1 (MUC1) is an epithelial mucin glycoprotein that is overexpressed in 90% of all adenocarcinomas including breast, lung, pancreas, prostate, stomach, colon, and ovary. MUC1 is a target for immune intervention, because, in patients with solid adenocarcinomas, low-level cellular and humoral immune responses to MUC1 have been observed, which are not sufficiently strong to eradicate the growing tumor. The hypothesis for this study is that enhancing MUC1-specific immunity will result in antitumor immunity. To test this, the authors have developed a clinically relevant breast cancer model that demonstrates peripheral and central tolerance to MUC1 and develops spontaneous tumors of the mammary gland. In these mice, the authors tested a vaccine formulation comprised of liposomal-MUC1 lipopeptide and human recombinant interleukin-2. Results indicate that when compared with untreated mice, immunized mice develop T cells that express intracellular IFN-gamma, are reactive with MHC class I H-2Db/MUC1 tetramer, and are cytotoxic against MUC1-expressing tumor cells in vitro. The presence of MUC1-specific CTL did not translate into a clinical response as measured by time of tumor onset, tumor burden, and survival. The authors demonstrate that some of the immune-evasion mechanisms used by the tumor cells include downregulation of MHC-class I molecule, expression of TGF-beta2, and decrease in IFN-gamma -expressing effector T cells as tumors progress. Finally, utilizing an injectable breast cancer model, the authors show that targeting a single tumor antigen may not be an effective antitumor treatment, but that immunization with dendritic cells fed with whole tumor lysate is effective in breaking tolerance and protecting mice from subsequent tumor challenge. A physiologically relevant spontaneous breast cancer model has been developed to test improved immunotherapeutic approaches.

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