Spontaneous pregnancy in postmenopausal women.
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Biomedical subjects
Publications and source records attributed to P Bamford.
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The mentoring connections that we have experienced in our school of nursing have eased difficult situations and have promoted self-awareness, personal and professional growth, and leadership behaviors. Various circumstances result in behaviors reflective of issues of culture, race, self-esteem and knowledge, values, ethics, experience, and conflict management. Some of these issues are related to oppressed group behavior, inadequate communication and conflict resolution skills, lack of exposure to diverse academic and professional experiences, and a need to learn management of feelings in effective ways. As faculty, administrators, students, and alumni, we struggle with those issues, knowing that resolution of them is beyond the traditional modes of teaching-learning, academic relationships and professional socialization. We wish that we and our students and alumni will experience an increased connectedness to the school and profession. We also wish that we might, as a result of our mentor connections, individually and collectively develop self-determination, self-esteem and confidence, leadership skills, and inner directness. The Mentor Connection Program was initiated in response to these strong wishes and has been a motivating framework for the reciprocal growth in us all. As for the future, we will continue our research and evaluation studies, refine the matching criteria, support and expand the mentoring dyads, strengthen faculty-faculty mentoring relationships, and seek funding resources for expansion and research. We are seeing the positive effects of active mentoring on students, faculty, and alumni on issues related to teaching and learning, support, hardiness, and self-reflection. Mentors produce leaders. Nursing's collective leadership will, we believe, depend to a large extent on our mentoring relationships with each other.
Necrotizing enterocolitis (NEC) is a serious gastrointestinal disorder of preterm infants. Other than an association with prematurity and gastrointestinal feeding, no single factor or mechanism has been consistently linked to this disease. We have previously demonstrated that Escherichia coli isolates obtained from the stool of infants with NEC caused NEC-like injury in a weanling rabbit ileal loop model; this injury, in turn, could be blocked by coinfection with selected Gram(+) bacteria (Enterococcus faecium) isolated from asymptomatic controls. Using Caco-2 cells in a trans-well system, we now demonstrate that the same E. coli isolates can cross epithelial cell monolayers in the absence of ultrastructural change or damage. These results with E. coli contrast with those seen with Salmonella typhimurium, which passed through the monolayer at a higher rate and were associated with striking ultrastructural damage. Transcytosis of E. coli was reduced 3-5-fold in the presence of E. faecium previously shown to block NEC-like injury in the loop model. There was a mild increase in the rate of E. coli transcytosis when studies were conducted with younger, undifferentiated cells; these immature cells had no brush border, had decreased production of brush border-specific enzymes, but retained well defined tight junctions, as demonstrated by transepithelial electrical resistance and electron microscopy. A further reduction/ complete blockage of E. coli transcytosis was observed when E. faecium was used as the coinfectant in studies with these undifferentiated cells. We hypothesize that the ability of E. coli to cross epithelial cell layer is a critical initial step in the cascade of events which lead ultimately to NEC; blockage or reduction in E. coli transcytosis in the presence of certain Gram(+) organisms may play a significant role in prevention of NEC.
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BACKGROUND: L-Glutamine is the principal energy source for small intestinal enterocytes. Diminution of intestinal function, mucosal atrophy, and increased bacterial translocation have been noted during total parenteral nutrition (TPN). In a rat model of glutamine starvation, we previously showed that luminal glutamine is essential for optimal intestinal function. In this study, we examined the effect of apical vs basolateral glutamine on bacterial translocation in a Caco-2 cell culture system and bacteria-induced tissue injury in a weanling rabbit ileal loop model. METHODS: Caco-2 cells were grown in a transwell system. After confluence, apical and basolateral chambers received defined media, and glutamine deprivation was carried out over a 4- to 48-hour period. Escherichia coli transcytosis and structure/function studies were then performed. In a second series of experiments, the effect of intraluminal glutamine supplementation was evaluated in an E. coli-induced tissue injury model in weanling rabbit ileal loops. RESULTS: Expression of disaccharidases, glucoamylase, and Na+/K(+)-adenosine 5'-triphosphatase (ATPase) were significantly reduced when cells were deprived of glutamine from the apical side, and there was increased bacterial translocation across the monolayer. Transepithelial epithelial resistance (TEER) across the monolayer was also reduced in the glutamine-free cultures. Glutamine replenishment over 24 to 48 hours restored the original functions. Basolateral deprivation had a smaller effect on the Caco-2 cells. Typical necrotic mucosal injury caused by E. coli in the ileal loops was blocked by co-infiltration of the loops with glutamine. CONCLUSIONS: This study demonstrates for the first time that the supply of glutamine from the apical side is of critical importance for maintaining optimal structure and function of the enterocytes. The effects are not acute or energy related. These observations have important clinical implications in the management of patients under critical care, including premature infants and patients receiving TPN, for whom lack of glutamine from the luminal side could produce mucosal dysfunction, resulting ultimately in severe atrophic/necrotic complications.