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Objective To describe the use of social media during the antepartum and postpartum periods among first-time African American mothers and their support persons. Design A qualitative critical ethnographic research design within the contexts of Family Life Course Development Theory and Black Feminist Theory. Setting Participants were recruited from community-based, public health, and home visiting programs. Participants A purposive sample was recruited, consisting of 14 pregnant African American women and eight support persons. Methods Pregnant and postpartum African American women and their support persons were interviewed separately during the antepartum and postpartum periods. Data were analyzed thematically. Results Participants frequently used social media for educational and social support and searched the internet for perinatal and parenting information. Most participants reported using at least one mobile application during their pregnancies and after giving birth. Social media were typically accessed through smartphones and/or computers using different websites and applications. While participants gleaned considerable information about infant development from these applications, they had difficulty finding and recalling information about infant feeding. Conclusion Social media are an important vehicle to disseminate infant feeding information; however, they are not currently being used to full potential. Our findings suggest that future interventions geared towards African American mothers and their support persons should include social media approaches. The way individuals gather, receive, and interpret information is dynamic. The increasing popularity and use of social media platforms offers the opportunity to create more innovative, targeted mobile health interventions for infant feeding and breastfeeding promotion.

Tai Chi was a culturally appropriate mind-body exercise for these older adults, with statistically significant psychosocial benefits observed over 12-weeks. Further research examining Tai Chi exercise using a randomized clinical trial design with an attention-control group may reduce potential confounding effects, while exploring potential mechanisms underlying the relaxation response associated with mind-body exercise. In addition, future studies with people with other chronic illnesses in all ethnic groups are recommended to determine if similar benefits can be achieved.

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Platelet-derived growth factor (PDGF) and sphingosine 1-phosphate (S1P) act via PDGF␤ receptor-S1P 1 receptor complexes in airway smooth muscle cells to promote mitogenic signaling. Several lines of evidence support this conclusion. First, both receptors were co-immunoprecipitated from cell lysates with specific anti-S1P 1 antibodies, indicating that they form a complex. Second, treatment of airway smooth muscle cells with PDGF stimulated the phosphorylation of p42/p44 MAPK, and this phosphorylated p42/p44 MAPK associates with the PDGF␤ receptor-S1P 1 receptor complex. Third, treatment of cells with antisense S1P 1 receptor plasmid construct reduced the PDGF-and S1P-dependent activation of p42/p44 MAPK. Fourth, S1P and/or PDGF induced the formation of endocytic vesicles containing both PDGF␤ receptors and S1P 1 receptors, which was required for activation of the p42/ p44 MAPK pathway. PDGF does not induce the release of S1P, suggesting the absence of a sequential mechanism. However, sphingosine kinase 1 is constitutively exported from cells and supports activation of p42/p44 MAPK by exogenous sphingosine. Thus, the presentation of sphingosine from other cell types and its conversion to S1P by the kinase exported from airway smooth muscle cells might enable S1P to act with PDGF on the PDGF␤ receptor-S1P 1 receptor complex to induce biological responses in vivo. These data provide further evidence for a novel mechanism for G-protein-coupled receptor and receptor tyrosine kinase signal integration that is distinct from the transactivation of receptor tyrosine kinases by G-proteincoupled receptor agonists and/or sequential release and action of S1P in response to PDGF. Sphingosine 1-phosphate (S1P)1 is a bioactive lysolipid that has been proposed to have both intracellular and extracellular actions (1). To date, five closely related G-protein-coupled receptors (GPCR), termed S1P 1 -S1P 5 (2) (and formerly named EDG1, EDG5/AGR16/H218, EDG3, EDG6 and EDG8/nrg-1, respectively) have been identified as high affinity S1P receptors (3-9). Further characterization studies confirmed the S1P 1 receptor to be a GPCR with high affinity for S1P that stimulates p42/p44 MAPK and inhibits adenylyl cyclase in cells (10 -13). The S1P 2 and S1P 3 receptors also have high affinity for S1P (14) and are linked via G q to phospholipase C and calcium mobilization and p42/p44 MAPK activation (14, 15) and via G 12 and G 13 to Rhoguanine nucleotide factor and Rho activation. The S1P 4 receptor is lymphoid specific and, in common with the S1P 5 receptor, uses G i/o and G 12 to signal (6, 8).The S1P 1 receptor is implicated in regulating smooth muscle cell migration, proliferation, and vascular maturation. Insight into the function of the S1P 1 receptor was obtained by studies showing that disruption of the s1p 1 gene by homologous recombination in mice results in extensive intra-embryonic hemorrhaging and intrauterine (16). This is caused by incomplete vascular maturation due to the failure of mural cells, vascular smooth muscle cells, and per...

The hypothesis that L-DOPA therapy in Parkinson's disease may augment neuronal damage and thus accelerate the progression of the disease remains controversial. In this study, we demonstrate that L-DOPA induces death of catecholaminergic cells in vitro via an active program of apoptosis. Treatment of PC12 cells with clinically applicable concentrations of L-DOPA (25-100 ,uM) induced cell death via a mechanism which exhibited morphological and biochemical characteristics of apoptosis, including chromatin condensation, membrane blebbing, and internucleosomal DNA fragmentation. L-DOPA-induced apoptosis was cell and drugtype specific. Toxicity is an intrinsic property of the drug molecule since it was not suppressed by inhibiting conversion of L-DOPA to dopamine. However, L-DOPA toxicity was inhibited by antioxidants, suggesting that activation of apoptosis is mediated by oxygen radicals. Our finding that L-DOPA-induced cell death in vitro occurs via apoptosis explains the lack of evidence supporting its toxicity in vivo, since apoptotic neurons are rapidly phagocytosed in vivo without causing damage to surrounding tissue. Furthermore, since apoptosis is an active cellular program which can be modulated, we suggest clinical approaches for decreasing L-DOPA toxicity, thus preventing acceleration of neuronal damage in Parkinson's disease. (J. Clin. Invest. 1995Invest. . 95:2458Invest. -2464

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