This paper introduces "Rip" a monoclonal antibody that produces relatively complete staining of oligodendrocytes and their processes in the adult central nervous system (CNS). The distribution of Rip immunoreactivity coincides with that of myelinated axons in both the spinal cord and the cerebellum. In addition, double-immunolabeling experiments demonstrate that Rip stains processes containing myelin basic protein but does not stain processes that express glial fibrillary acidic protein. These results indicate that Rip selectively stains oligodendrocytes but not astrocytes. Moreover, individual Rip-stained oligodendrologial somata and their cytoplasmic processes were observable at both the light microscopic and electron microscopic level when the staining of myelin was reduced. This was accomplished by omitting detergents from antibody incubation steps. Rip-stained oligodendrocytes have multiple processes of varying thickness, some of which end in close proximity to myelin sheaths. These immunostained profiles, reminiscent of those observed in oligodendrocytes stained by Golgi methods, are unique to Rip and indicate that its immunoreactivity is distinct from that of existing serological markers for oligodendrocytes.

Framing battles in public health illustrate the tension in our society between individual freedom and collective responsibility. This article describes how two frames, market justice and social justice, first articulated in a public health context by Dan Beauchamp, influence public dialogue on the health consequences of corporate practices. The authors argue that public health advocates must articulate the social justice values motivating the changes they seek in specific policy battles that will be debated in the context of news coverage. The authors conclude with lessons for health education practitioners who need to frame public health issues in contentious and controversial policy contexts. Specific lessons include the importance of understanding the existing values and beliefs motivating the public health change being sought, the benefits of articulating core messages that correspond to shared values, and the necessity of developing media skills to compete effectively with adversaries in public debate.

Diabetes is a chronic disease associated with hyperglycemia and altered bone metabolism that may lead to complications including osteopenia, increased risk of fracture and osteoporosis. Hyperglycemia has been implicated in the pathogenesis of diabetic bone disease; however, the biologic effect of glucose on osteoclastogenesis is unclear. In the present study, we examined the effect of high D(+)glucose (D-Glc) and L(−)glucose (L-Glc; osmotic control) on RANKL-induced osteoclastogenesis using RAW264.7 cells and Bone Marrow Macrophages (BMM) as models. Cells were exposed to sustained high glucose levels to mimic diabetic conditions. Osteoclast formation was analyzed using tartrate resistant acid phosphatase (TRACP) assay, expression of calcitonin receptor (CTR) and cathepsin K mRNAs, and cultures were examined for reactive oxygen species (ROS) using dichlorodihydrofluorescein diacetate (DCF-DA) fluorescence, caspase-3 and Nuclear Factor kappaB (NF-κB) activity. Cellular function was assessed using a migration assay. Results show, for the first time, that high D-Glc inhibits osteoclast formation, ROS production, caspase-3 activity and migration in response to RANKL through a metabolic pathway. Our findings also suggest that high D-Glc may alter RANKL-induced osteoclast formation by inhibiting redox-sensitive NF-κB activity through an anti-oxidative mechanism. This study increases our understanding of the role of glucose in diabetes-associated bone disease. Our data suggest that high glucose levels may alter bone turnover by decreasing osteoclast differentiation and function in diabetes and provide new insight into the biologic effects of glucose on osteoclastogenesis.

The molecular mechanism for the beneficial effect of fish oil on breast tumor growth is largely undefined. Using the xenograft model in nude mice, we for the first time report that the fish oil diet significantly increased the level of PTEN protein in the breast tumors. In addition, the fish oil diet attenuated the PI 3 kinase and Akt kinase activity in the tumors leading to significant inhibition of NFκB activation. Fish oil diet also prevented the expression of anti-apoptotic proteins Bcl-2 and Bcl-XL in the breast tumors with concomitant increase in caspase 3 activity. To extend these findings we tested the functional effects of DHA and EPA, the two active ω-3 fatty acids of fish oil, on cultured MDA MB-231 cells. In agreement with our in vivo data, DHA and EPA treatment increased PTEN mRNA and protein expression and inhibited the phosphorylation of p65 subunit of NFκB in MDA MB-231 cells. Furthermore, DHA and EPA reduced expression of Bcl-2 and Bcl-XL. NFκB DNA binding activity and NFκB-dependent transcription of Bcl-2 and Bcl-XL genes were also prevented by DHA and EPA treatment. Finally, we showed that PTEN expression significantly inhibited NFκB-dependent transcription of Bcl-2 and Bcl-XL genes. Taken together, our data reveals a novel signaling pathway linking the fish oil diet to increased PTEN expression that attenuates the growth promoting signals and augments the apoptotic signals, resulting in breast tumor regression.