Crohn's disease is an inflammatory bowel disease associated with substantial morbidity. Complications arising from this disease affect many organ systems. In particular, hepatitis, pancreatitis, blood dyscrasias, and renal disease are believed to occur more frequently in patients with Crohn's disease. The incidence of these conditions is also believed to be increased by some of the medications used to treat Crohn's disease. Sulfasalazine as well as mesalamine have been associated with hepatitis, pancreatitis, renal disease, and blood dyscrasias. In addition to characterizing the demographics and severity of Crohn's disease in Saskatchewan, the purpose of this study was also to determine if, in patients with Crohn's disease, there is an increased risk of developing these adverse conditions associated with the medications used to treat this condition. In this study 1999 patients with Crohn's disease who met inclusion criteria, were identified in the Saskatchewan Healthcare datafiles. (Abstract shortened by UMI.)

A survey was undertaken to assess the knowledge, attitudes and practices, with respect to malaria, of 300 women from six randomly selected rural communities in Central Ethiopia from December 1991 to February 1992. Eighty-five per cent were able to recognize one or more of the common symptoms of malaria. Transmission was generally misunderstood and only 23% believed it could be prevented. More women preferred to obtain antimalarials from government clinics than from private drug shops, mission clinics, unofficial injectors, open markets or from leftover sources. Children under five were identified as the most malaria-vulnerable group and given priority for treatment. Severity of illness was the principal determinant in seeking treatment. Decisions were generally made jointly by both parents. / As distance from a health unit increased, knowledge about transmissibility of malaria decreased (OR =.48; 95% CI.27,.86). Logistic regression analysis showed literacy and village to be the most important variables associated with knowledge of prevention.

Thesis (Ph.D.)--Indiana University, Dept. of History, 2008. / Title from home page (viewed on May 11, 2009). Source: Dissertation Abstracts International, Volume: 69-08, Section: A, page: 3277. Adviser: John H. Hanson.

Thesis (Ph.D.)--University of California, San Francisco, 2006. / Source: Dissertation Abstracts International, Volume: 67-05, Section: B, page: 2498. Adviser: Leslie Z. Benet.

Hepatitis C virus (HCV) is the etiologic agent responsible for the majority of cases of non-A, non-B hepatitis. It is estimated that 2% of the world's population is infected with hepatitis C with roughly 75% of infections progressing into a chronic state. Current interferon therapy is largely ineffective against chronic Hepatitis C due to the induction of interferon-resistance by HCV. The underlying mechanisms for resistance to interferon therapy have been widely studied and documented and as is the case in interferon resistant malignancies, there is some evidence that HCV infected cells are more susceptible to infection by interferon sensitive viruses. Most current research into novel HCV therapeutics has focused on the discovery of inhibitors of viral replication. However, the high mutation rate of the HCV genome makes it a virtual certainty that viral variants resistant to protease and/or polymerase inhibitors will arise. As an alternative approach, we have designed a therapeutic strategy that exploits both the expression of a viral protease in infected cells as well as the defects in the interferon pathway to build selectively active therapeutics that target and kill HCV infected cells. Initial experiments showed some promise using this approach and indicated areas for further development. Conditionally replicating viruses failed to rescue in HCV expressing cell lines, thus requiring further modification. A separate approach involving conditional stabilization of the suicide gene HSV-1 TK was successful with a two-fold increase in the expression levels of TK in cells co-expressing HCV protease.

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