Student Learning in an Accelerated Introductory Biology Course Is Significantly Enhanced by a Flipped-Learning Environment.

A flipped-classroom environment generally strives to create more in-class time for activities that enhance student learning, while shifting some content delivery to outside the classroom through the use of short didactic videos. We compared a flipped-classroom setting with the traditional ("control") setting for an accelerated lower-division general biology course. Student self-reporting and video analytics functions showed ample and variable video viewing among individual students.

No significant CTL cross-priming by dendritic cell-derived exosomes during murine lymphocytic choriomeningitis virus infection.

Exosomes are small membrane vesicles of endocytic origin that are secreted by most cells in culture, but are also present in serum. They contain a wide array of protein ligands on their surface, which has led to the hypothesis that they might mediate intercellular communication. Indeed, data support that exosomes can transfer Ags to dendritic cells (DC), and, interestingly, that these DC can subsequently induce T cell priming or tolerance.

Redox-signaling transmitted in trans to neighboring cells by melanoma-derived TNF-containing exosomes.

Hydrogen peroxide is known to be involved in redox signaling pathways that regulate normal processes and disease progression, including cytokine signaling, oxidative stress, and cancer. In studies on immune surveillance against cancer, hydrogen peroxide was found to disrupt cytotoxic T-cell function, thus contributing to tumor escape. In this study, secretion of TNF-containing vesicles of rab9+ endosomal origin, termed exosomes, was investigated using GFP-TNF constructs.

SOCS-1 protects from virally-induced CD8 T cell mediated type 1 diabetes.

CD8(+) cytotoxic T lymphocytes (CTL) can rapidly kill beta-cells and therefore contribute to the development of type 1 diabetes (T1D). CTL-mediated beta-cell killing can occur via perforin-mediated lysis, Fas-Fas-L interaction, and the secretion of TNF-alpha or IFN-gamma. The secretion of IFN-gamma can contribute to beta-cell death directly by eliciting nitric oxide production, and indirectly by upregulating MHC class I and 'unmasking' beta-cells for recognition by CTL.

Islet-specific expression of CXCL10 causes spontaneous islet infiltration and accelerates diabetes development.

During inflammation, chemokines are conductors of lymphocyte trafficking. The chemokine CXCL10 is expressed early after virus infection. In a virus-induced mouse model for type 1 diabetes, CXCL10 blockade abrogated disease by interfering with trafficking of autoaggressive lymphocytes to the pancreas.