Library, Media, Web Services Annual Report 2006-07

This report is the first report of the merged organization that includes the DeWitt Wallace Library, Media Services, and campus Web Services. It is a summary of activities and statistics for the academic year 2006-07. This report is a collaborative effort by the entire staff and features highlights including new services, new people, new collections, new spaces, new technologies, and celebrations

DeWitt Wallace Library Biennial Report 2007-2009

This report summarizes the activities in the DeWitt Wallace Library for the years 2007-09. This report is a collaborative effort by the entire staff and features highlights including new services, new people, new collections, new spaces, new technologies, and celebrations

STAT3 in the systemic inflammation of cancer cachexia

Weight loss is diagnostic of cachexia, a debilitating syndrome contributing mightily to morbidity and mortality in cancer. Most research has probed mechanisms leading to muscle atrophy and adipose wasting in cachexia; however cachexia is a truly systemic phenomenon. Presence of the tumor elicits an inflammatory response and profound metabolic derangements involving not only muscle and fat, but also the hypothalamus, liver, heart, blood, spleen and likely other organs. This global response is orchestrated in part through circulating cytokines that rise in conditions of cachexia. Exogenous Interleukin-6 (IL6) and related cytokines can induce most cachexia symptomatology, including muscle and fat wasting, the acute phase response and anemia, while IL-6 inhibition reduces muscle loss in cancer. Although mechanistic studies are ongoing, certain of these cachexia phenotypes have been causally linked to the cytokine-activated transcription factor, STAT3, including skeletal muscle wasting, cardiac dysfunction and hypothalamic inflammation. Correlative studies implicate STAT3 in fat wasting and the acute phase response in cancer cachexia. Parallel data in non-cancer models and disease states suggest both pathological and protective functions for STAT3 in other organs during cachexia. STAT3 also contributes to cancer cachexia through enhancing tumorigenesis, metastasis and immune suppression, particularly in tumors associated with high prevalence of cachexia. This review examines the evidence linking STAT3 to multi-organ manifestations of cachexia and the potential and perils for targeting STAT3 to reduce cachexia and prolong survival in cancer patients

DeWitt Wallace Library Annual Report 2013-2014

Summary of library and media services activities for 2013-201