Maternity Experiences and Perceptions of Emergency Medicine Physicians.

INTRODUCTION: Postpartum employment has been recognized as a significant obstacle to breastfeeding continuation rates in the general population. Multiple additional factors can influence emergency medicine (EM) physician mothers' ability to continue breastfeeding upon return to work. These include the unpredictable nature of emergency room volumes and acuity, absence of protected lactation time or facilities, and varying levels of support from colleagues. This study investigated a sample of female EM physicians' current perceptions and experiences regarding breastfeeding practices and identified modifiable work-place factors affecting their decision to wean. The authors hypothesized that EM physician mothers would have excellent breastfeeding initiation rates but be largely unable to maintain breastfeeding practices upon returning to work. METHODS: A 34-item survey questionnaire evaluated demographics, perceptions, and experiences with breastfeeding with a convenience sample of EM attending and resident physicians from two Michigan academic community hospitals. RESULTS: Thirty-nine surveys were completed, representing a participant response rate of 88.6%. Breastfeeding had been initiated by all respondent mothers, all of whom returned to full-time employment after delivery. Upon return to work, 15 (75%) respondents continued to exclusively breastfeed. The goal of participants was to breastfeed for an average of 7.1 months (± 4.1 months), although the average duration children were exclusively breastfed was 5.8 months (± 4.0 months). CONCLUSIONS: Based on these results, the reasons for decreased breastfeeding after return to work in an EM residency program setting are multifactorial and include some modifiable interpersonal and institutional influences. These findings support the implementation of work-place strategies and policies to promote successful breastfeeding practices among EM resident and attending physician mothers returning to work.

Pressure overload generates a cardiac-specific profile of inflammatory mediators.

Mechanisms that contribute to myocardial fibrosis, particularly in response to left ventricular pressure overload (LVPO), remain poorly defined. To test the hypothesis that a myocardial-specific profile of secreted factors is produced in response to PO, levels of 44 factors implicated in immune cell recruitment and function were assessed in a murine model of cardiac hypertrophy and compared with levels produced in a model of pulmonary fibrosis (PF). Mice subjected to PO were assessed at 1 and 4 wk. Protein from plasma, LV, lungs, and kidneys were analyzed by specific protein array analysis in parallel with protein from mice subjected to silica-instilled PF. Of the 44 factors assessed, 13 proteins were elevated in 1-wk PO myocardium, whereas 18 proteins were found increased in fibrotic lung. Eight of those increased in 1-wk LVPO were not found to be increased in fibrotic lungs (CCL-11, CCL-12, CCL-17, CCL-19, CCL-21, CCL-22, IL-16, and VEGF). Additionally, six factors were increased in plasma of 1-wk LVPO in the absence of increases in myocardial levels. In contrast, in mice with PF, no factors were found increased in plasma that were not elevated in lung tissue. Of those factors increased at 1 wk, only TIMP-1 remained elevated at 4 wk of LVPO. Immunohistochemistry of myocardial vasculature at 1 and 4 wk revealed similar amounts of total vasculature; however, evidence of activated endothelium was observed at 1 wk and, to a lesser extent, at 4 wk LVPO. In conclusion, PO myocardium generated a unique signature of cytokine expression versus that of fibrotic lung.NEW & NOTEWORTHY Myocardial fibrosis and the resultant increases in myocardial stiffness represent pivotal consequences of chronic pressure overload (PO). In this study, cytokine profiles produced in a murine model of cardiac fibrosis induced by PO were compared with those produced in response to silica-induced lung fibrosis. A unique profile of cardiac tissue-specific and plasma-derived factors generated in response to PO are reported.

Bovine and human lactoferricin peptides: chimeras and new cyclic analogs.

Lactoferrin (LF) is an important antimicrobial and immune regulatory protein present in neutrophils and most exocrine secretions of mammals. The antimicrobial activity of LF has been related to the presence of an antimicrobial peptide sequence, called lactoferricin (LFcin), located in the N-terminal region of the protein. The antimicrobial activity of bovine LFcin is considerably stronger than the human version. In this work, chimera peptides combining segments of bovine and human LFcin were generated in order to study their antimicrobial activity and mechanism of action. In addition, the relevance of the conserved disulfide bridge and the resulting cyclic structure of both LFcins were analyzed by using "click chemistry" and sortase A-catalyzed cyclization of the peptides. The N-terminal region of bovine LFcin (residues 17-25 of bovine LF) proved to be very important for the antimicrobial activity of the chimera peptides against E. coli, when combined with the C-terminal region of human LFcin. Similarly the cyclic bovine LFcin analogs generated by "click chemistry" and sortase A preserved the antimicrobial activity of the original peptide, showing the significance of these two techniques in the design of cyclic antimicrobial peptides. The mechanism of action of bovine LFcin and its active derived peptides was strongly correlated with membrane leakage in E. coli and up to some extent with the ability to induce vesicle aggregation. This mechanism was also preserved under conditions of high ionic strength (150 mM NaCl) illustrating the importance of these peptides in a more physiologically relevant system.