Patient and Community Organization Perspectives on Accessing Social Resources from the Emergency Department: A Qualitative Study.

INTRODUCTION: Social risks adversely affect health and are associated with increased healthcare utilization and costs. Emergency department (ED) patients have high rates of social risk; however, little is known about best practices for ED-based screening or linkage to community resources. We examined the perspectives of patients and community organizations regarding social risk screening and linkage from the ED. METHODS: Qualitative interviews were conducted with a purposive sample of ED patients and local community organization staff. Participants completed a brief demographic survey, health literacy assessment, and qualitative interview focused on barriers/facilitators to social risk screening in the ED, and ideas for screening and linkage interventions in the ED. Interviews were conducted in English or Spanish, recorded, transcribed, and coded. Themes were identified by consensus. RESULTS: We conducted 22 interviews with 16 patients and six community organization staff. Three categories of themes emerged. The first related to the importance of social risk screening in the ED. The second category encompassed challenges regarding screening and linkage, including fear, mistrust, transmission of accurate information, and time/resource constraints. The third category included suggestions for improvement and program development. Patients had varied preferences for verbal vs electronic strategies for screening. Community organization staff emphasized resource scarcity and multimodal communication strategies. CONCLUSION: The development of flexible, multimodal, social risk screening tools, and the creation and maintenance of an accurate database of local resources, are strategies that may facilitate improved identification of social risk and successful linkage to available community resources.

Interferon-γ protects first-trimester decidual cells against aberrant matrix metalloproteinases 1, 3, and 9 expression in preeclampsia.

Human extravillous trophoblast (EVT) invades the decidua via integrin receptors and subsequently degrades extracellular matrix proteins. In preeclampsia (PE), shallow EVT invasion elicits incomplete spiral artery remodeling, causing reduced uteroplacental blood flow. Previous studies show that preeclamptic decidual cells, but not interstitial EVTs, display higher levels of extracellular matrix-degrading matrix metalloproteinase (MMP)-9, but not MMP-2. Herein, we extend our previous PE-related assessment of MMP-2 and MMP-9 to include MMP-1, which preferentially degrades fibrillar collagens, and MMP-3, which can initiate a local proteolytic cascade. In human first-trimester decidual cells incubated with estradiol, tumor necrosis factor-α (TNF-α) significantly enhanced MMP-1, MMP-3, and MMP-9 mRNA and protein levels and activity measured by real-time quantitative RT-PCR, ELISA, immunoblotting, and zymography, respectively. In contrast, interferon γ (IFN-γ) reversed these effects and medroxyprogesterone acetate elicited further reversal. Immunoblotting revealed that p38 mitogen-activated protein kinase signaling mediated TNF-α enhancement of MMP-1, MMP-3, and MMP-9, whereas IFN-γ inhibited p38 mitogen-activated protein kinase phosphorylation. Unlike highly regulated MMP-1, MMP-3, and MMP-9, MMP-2 mRNA and protein expression was constitutive in decidual cells. Because inflammation underlies PE-associated shallow EVT invasion, these results suggest that excess macrophage-derived TNF-α augments expression of MMP-1, MMP-3, and MMP-9 in decidual cells to interfere with normal stepwise EVT invasion of the decidua. In contrast, decidual natural killer cell-derived IFN-γ reverses such TNF-α-induced MMPs to protect against PE.

Risk of placental abruption in relation to maternal depressive, anxiety and stress symptoms.

BACKGROUND: Little is known about the influence of psychiatric factors on the etiology of placental abruption (PA), an obstetrical condition that complicates 1-2% of pregnancies. We examined the risk of PA in relation to maternal psychiatric symptoms during pregnancy. METHODS: This case-control study included 373 PA cases and 368 controls delivered at five medical centers in Lima, Peru. Depressive, anxiety and stress symptoms were assessed using the Patient Health Questionnaire (PHQ-9) and the Depression Anxiety Stress Scales (DASS-21). Multivariable logistic regression models were fit to calculate odds ratios (aOR) and 95% confidence intervals (CI) adjusted for confounders. RESULTS: Depressive symptoms of increasing severity (using the DASS depression subscale) was associated with PA (p for trend=0.02). Compared with women with no depressive symptoms, the aOR (95%CI) for PA associated with each level of severity of depression symptoms based on the DASS assessment were as follows: mild 1.84 (0.91-3.74); moderate 1.25 (0.67-2.33); and severe 4.68 (0.98-22.4). The corresponding ORs for mild, moderate, and moderately severe depressive symptoms based on the PHQ assessment were 1.10 (0.79-1.54), 3.31 (1.45-7.57), and 5.01 (1.06-23.6), respectively. A positive gradient was observed for the odds of PA with severity of anxiety (p for trend=0.002) and stress symptoms (p for trend=0.002). LIMITATIONS: These cross-sectionally collected data may be subject to recall bias. CONCLUSIONS: Maternal psychiatric disorders may be associated with an increased occurrence of AP. Larger studies that allow for more precise evaluations of maternal psychiatric health in relation to PA risk are warranted.

Microvesicle entry into marrow cells mediates tissue-specific changes in mRNA by direct delivery of mRNA and induction of transcription.

OBJECTIVE: Microvesicles have been shown to mediate intercellular communication. Previously, we have correlated entry of murine lung-derived microvesicles into murine bone marrow cells with expression of pulmonary epithelial cell-specific messenger RNA (mRNA) in these marrow cells. The present studies establish that entry of lung-derived microvesicles into marrow cells is a prerequisite for marrow expression of pulmonary epithelial cell-derived mRNA. MATERIALS AND METHODS: Murine bone marrow cells cocultured with rat lung, but separated from them using a cell-impermeable membrane (0.4-microm pore size), were analyzed using species-specific primers (for rat or mouse). RESULTS: These studies revealed that surfactant B and C mRNA produced by murine marrow cells were of both rat and mouse origin. Similar results were obtained using murine lung cocultured with rat bone marrow cells or when bone marrow cells were analyzed for the presence of species-specific albumin mRNA after coculture with rat or murine liver. These studies show that microvesicles both deliver mRNA to marrow cells and mediate marrow cell transcription of tissue-specific mRNA. The latter likely underlies the longer-term stable change in genetic phenotype that has been observed. We have also observed microRNA in lung-derived microvesicles, and studies with RNase-treated microvesicles indicate that microRNA negatively modulates pulmonary epithelial cell-specific mRNA levels in cocultured marrow cells. In addition, we have also observed tissue-specific expression of brain, heart, and liver mRNA in cocultured marrow cells, suggesting that microvesicle-mediated cellular phenotype change is a universal phenomena. CONCLUSION: These studies suggest that cellular systems are more phenotypically labile than previously considered.