Fusion of Viral Proteins Apoptin and PCV-1 VP3 C-Terminus: A Study of Localization and Induced Specific Apoptosis of Carcinogenic Cells

Viral proteins Apoptin and PCV-1 VP3 selectively cause apoptosis in cancerous cells. The first 315 bps of PCV-1 VP3 share homology with apoptin, the second 306 bps (Tail), are non-homologous to apoptin. Apoptin undergoes nuclear localization in cancerous cells, where PCV-1 VP3 is cytoplasmically localized, due to a strong nuclear export sequence in the ‘Tail”. To determine if nuclear localization was necessary for apoptin to induce apotosis, the “Tail” of PCV-1 VP3 was fused to apoptin. The fused protein was transfected into H1299 lung cancer cells. Localization and apoptosis studies were done. It was found that the fused protein localized to the cytoplasm but did not induce apoptosis, implying that nuclear localization may be a critical step in the induction of apoptosis by apoptin

Effective Communication of Science and Engineering Breakthroughs to the Public: A Tool for Science and Engineering Professionals

The goal of our research was to gain an understanding of the problems of misinformation, linguistic misinterpretation, public comprehension, scientific justification, and audience gauging in presentation of research to the public. Surveys and Interviews were our primary means of gathering data. Language was one of the largest factors in misinterpretation. There is much discrepancy between what people think is a valid source and what the scientific community recognizes as a valid source. Ways of presenting data that scientists find easy to understand may be easily misunderstood by members of the public. These problems can often be avoided by properly tailoring one's presentation to one's audience

Altered Interleukin-10 Signaling in Skeletal Muscle Regulates Obesity-Mediated Inflammation and Insulin Resistance

Skeletal muscle insulin resistance is a major characteristic of obesity and type 2 diabetes. Although obesity-mediated inflammation is causally associated with insulin resistance, the underlying mechanism is unclear. Here, we examined the effects of chronic obesity in mice with muscle-specific overexpression of interleukin-10 (MIL10). After 16 weeks of a high-fat diet (HFD), MIL10 mice became markedly obese but showed improved insulin action compared to that of wild-type mice, which was largely due to increased glucose metabolism and reduced inflammation in skeletal muscle. Since leptin regulates inflammation, the beneficial effects of interleukin-10 (IL-10) were further examined in leptin-deficient ob/ob mice. Muscle-specific overexpression of IL-10 in ob/ob mice (MCK-IL10ob/ob) did not affect spontaneous obesity, but MCK-IL10ob/ob mice showed increased glucose turnover compared to that in ob/ob mice. Last, mice with muscle-specific ablation of IL-10 receptor (M-IL10R-/-) were generated to determine whether IL-10 signaling in skeletal muscle is involved in IL-10 effects on glucose metabolism. After an HFD, M-IL10R-/- mice developed insulin resistance with reduced glucose metabolism compared to that in wild-type mice. Overall, these results demonstrate IL-10 effects to attenuate obesity-mediated inflammation and improve insulin sensitivity in skeletal muscle, and our findings implicate a potential therapeutic role of anti-inflammatory cytokines in treating insulin resistance and type 2 diabetes