Purpose: The purpose of this study was to describe the experience of caring for women with a perinatal loss from the perspective of the nurse and to determine the extent to which the response to perinatal loss reflects a process. Study Design and Methods: A purposive study was conducted with nine labor and birth nurses with experience in caring for women with a perinatal loss. The nurses were from two acute care hospitals within one healthcare system in Southeastern Massachusetts. A qualitative descriptive design with in-depth interviewing based on Rubin and Rubin (2012) was used to gather and analyze data. Results: Several themes depicting nurses' experience were identified: struggling with emotions, carrying on in the moment, being present for the patient, expressing conflict, and taking care of self. A process was identified by nurses describing their response to perinatal loss. The process began with recognition of the loss and progressed through phases including the recognition of their emotional impact, connecting with the mother, dealing with emotions, acting professionally, preparing to return to work, and never forgetting the woman. Clinical Implications: Nurses identified a need for more education and managerial support for excellence in care of women with a perinatal loss. Education to prepare nurses to meet the physical, psychological, and spiritual needs of women is recommended. Debriefing after caring for a woman with a loss was suggested by the nurses. When nurses' needs are met, they are better prepared to care for women experiencing a perinatal loss.
Among characterized forms of liver microsomal cytochromes P450 in rats are four related isozymes (P450f-i) notable for their lack of inducibility. Immunoblot analyses demonstrated that human livers microsomes contained several proteins related to these rat P450s. A human liver P450, termed HLx, was purified and found by immunochemical assays to resemble rat P450g. Analysis of the NH2-terminal amino acid sequence of HLx indicates that it is related to rat P450s f-i and human liver P45OMP. A monoclonal antibody was used to measure the amounts of HLx in 21 human liver specimens. No correlation between the levels of HLx protein in these specimens and the patients' environmental histories was observed. However, statistical analysis of the data suggests that the distribution of HLx is at least bimodal. We conclude that HLx is a member of a family of human liver P-450s that resembles in its structure, and possibly in its distribution, several liver P450s found in other animals.
The contributions of insulin (IRI), glucagon (IRG), and corticosterone production to the glycemic changes associated with age and starvation were examined in 3 and 6 month old ob/ob and lean mice. Three month old ob/ob mice had elevated glucose levels under all feeding conditions, but in older obese mice basal hyperglycemia was evident only after 48 hours of food deprivation. These age differences in glycoregulation were not consistently related to changes of IRI, IRG, or corticosterone concentrations. Similarly, the mild diabetes associated with senescence in lean mice was only evident during food deprivation. This abnormality in glycoregulation was also independent of decreased IRI or elevated diabetogenic hormone concentrations. Our results indicate that there is no simple hormonal basis for the partial remission of diabetes in older ob/ob mice, or for the development of mild diabetes in aging lean mice. Additionally, these data suggest that the tissue 'resistance' that is associated with chronic insulin overproduction might also develop in response to persistent overproduction of other metabolically-active hormones.
The effect of ventromedial (VMN) or basolateral (LHA) hypothalamic electrical stimulation on glucose and hormone production was examined in conscious and anesthetized male rats. Barbiturate treatment alone led to large increases of corticosterone and smaller but significant increases of glucose, insulin, and glucagon. When hypothalamic stimulation was combined with anesthesia, interactions between the hypothalamic sites and the awake-anesthetized conditions were observed. This was most evident with LHA placements, as awake rats exhibited mild hypoglycemia and hypoglucagonemia in response to low-level (approximately 10 microA rms) current, but no effects on these values were seen with VMN electrodes. With barbiturate anesthesia, the same level of stimulation led to severe hyperglycemia in both VMN and LHA rats and a mild hyperglucagonemia in the LHA group. No consistent effects of stimulation on immunoreactive insulin or corticosterone were detected at either hypothalamic site or in any anesthesia condition. The present results point out the important role anesthetics may play in studies defining functional aspects of the hypothalamus. Furthermore, our inability to elicit consistent autonomic responses with electrical stimulation, when compared with the effectiveness of both metabolic agents and pharmacologic stimuli, suggests that the sites integrating autonomic function may be diffusely distributed over the basal diencephalon.
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