Alexandersenjohnson0779

Recent literature on the public understanding of science has focused on replacing the deficit model of public communication in which experts disseminate information with one that encourages public participation and dialogue. Situated within this call for increased participation, this study looks at self-care practices in which medical expertise is not passively consumed by the layperson, but shared and (re)produced through arenas of lay practice. This collective knowledge production is facilitated by the online environment, which provides access to mediated medical knowledge and the ability to form communities in which users can negotiate this expertise and share their experiences. The laypersons examined here are members of the Canadian online collective, Running Mania, highlighting how this negotiation of expertise occurs in a "wellness" community. Drawing from member interviews and website observations of the site's injury forum, the study examines collective injury management using two dominant theoretical discourses surrounding lay knowledge and participation in medical expertise the lay expert whose knowledge arises from experience and the expert patient whose knowledge base parallels dominant biomedical discourse. Using the coproduction model and the related concepts of tinkering and logic of care from material semiotics, the research examines how these knowledge forms articulate to produce an intermediary discourse unique to this collective's articulation of running and caring practices, a discourse that is enacted in individuals' embodied negotiation of these multiple forms of medical expertise. It suggests that the logic of care has the potential to bridge the expert/lay boundary since the need for persistent, attentive tinkering applies across epistemological divides in "good" care practices, multiple expertises are needed, both expert and lay, to hold the body together.

Circ_0015382 expression was found to be up-regulated in preeclampsia (PE) placenta tissues, while the role and molecular mechanisms of circ_0015382 in PE remain unclear.

The expression of circ_0015382, microRNA (miR)-149-5p, and tissue factor pathway inhibitor 2 (TFPI2) was measured using quantitative real-time polymerase chain reaction and Western blot. Cell proliferation, migration, invasion, apoptosis, and cell cycle, were detected using cell counting kit-8, transwell, and flow cytometry assays, respectively. The direct interaction between miR-149-5p and circ_0015382 or TFPI2 was analyzed using the dual-luciferase reporter assay.

Circ_0015382 was highly expressed in placental tissues of PE. Overexpression of circ_0015382 suppressed trophoblast cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT), but induced apoptosis and cell cycle progression, while circ_0015382 knockdown showed inverse effects. MiR-149-5p was confirmed to be a target of circ_0015382, and silencing miR-149-5p reversed the regulatory effects of circ_0015382 knockdown on trophoblast cell biological behaviors. MiR-149-5P was expressed at lower levels in placental tissues of PE, while the expression of its target TFPI2 was higher. Importantly, circ_0015382 could regulate TFPI2 expression via miR-149-5p. Additionally, miR-149-5p was shown to promote trophoblast cell growth, migration, invasion and EMT through TFPI2.

Circ_0015382 was associated with the onset and development of PE through suppressing trophoblast cell growth, migration, invasion and EMT via miR-149-5p/TFPI2 axis, revealing a new insight into the pathogenesis of PE and a potential therapeutic target for PE treatment.

Circ_0015382 was associated with the onset and development of PE through suppressing trophoblast cell growth, migration, invasion and EMT via miR-149-5p/TFPI2 axis, revealing a new insight into the pathogenesis of PE and a potential therapeutic target for PE treatment.

The human placenta expresses multiple glucocorticoid receptor (GR) isoforms that may be partially regulated by the untranslated 5' exon 1GR gene promoter region which consists of 9 different promoters and 13 splice variants. The objective of this study was to determine which GR exon 1 variants are expressed in the human placenta and relate these findings to GR mRNA and protein expression.

Placental extracts from pregnancies with or without the complication of maternal asthma and trophoblast cells exposed to an inflammatory challenge in vitro were examined using PCR and Western blot to measure GR exon 1 variants, GR splice variant mRNA and GR protein isoforms, respectively.

All 9GR exon 1 variants were detectable in the human placenta and included GR exons 1A, 1B, 1C, 1D, 1E, 1F, 1H, 1I and 1J. In the presence of maternal asthma and a male fetus there was preferential expression of GR exon 1B, 1C, IF and 1J (KW-ANOVA, P<0.05) which were positively correlated with GRα D3 protein isoform. read more In female placentae from pregnancies complicated by asthma there was no upregulation of any exon 1 variant (KW-ANOVA, P<0.05). Exposure of BeWo trophoblast cell line to an inflammatory challenge, lipopolysaccharide, in vitro, resulted in preferential expression of GR exon 1B, 1D, 1E and 1H and associated with GRα-D1 protein upregulation.

The preferential expression of different GR exon 1 promoters drive the upregulation of GRα D isoforms and contribute to glucocorticoid resistance observed in male placentae of pregnancies complicated by asthma.

The preferential expression of different GR exon 1 promoters drive the upregulation of GRα D isoforms and contribute to glucocorticoid resistance observed in male placentae of pregnancies complicated by asthma.

The maternal part of the rodent placenta harbors a circadian clock which robustly responds to glucocorticoids, however, its sensitivity to other hormones has not been elucidated. In this study, we tested five selected hormones (dopamine, melatonin, insulin, leptin and ghrelin) for their effectiveness to affect the clock in decidual region of mouse placenta in vitro.

We administered the hormones or corresponding vehicles at various time points over 24h to organotypic placental explants of mPer2

mice containing the decidua basalis (DB) region and monitored their effects on amplitude, period, median expression level (mesor) and phase of PER2-driven bioluminescence rhythms.

Dopamine significantly increased the amplitude, robustly dampened the mesor, and during a narrow time interval (corresponding to daytime) induced phase delays of the rhythms. In contrast, melatonin had no effect on amplitude, but induced phase advances of the rhythms at the opposite time window than dopamine (corresponding to nighttime).