Postnatal Depression: Its Nature,Effects, and Identification Using the Edinburgh Postnatal Depression Scale

ABSTRACT: Postnatal depression, or clinical depression in mothers during the months after childbirth, occurs at a time when heavy demands are placed on these women's resources, and when infant learning and development are taking place. Identification and treatment are facilitated when health professionals and services are in close contact with the family and can provide beneficial intervention. Two studies examined whether women with nonpsychotic postnatal depression could be recognized and treated within existing services, using the Edinburgh Postnatal Depression Scale and a randomized, controlled trial of counseling intervention with health visitors.     

Clinical support and the Project 2000 nursing student: factors influencing this process

This paper reports on research commissioned by the English National Board for Nursing, Midwifery and Health Visiting into mentorship and clinical support arrangements for Project 2000 nursing students in the adult and mental health branches Interviews and observation data were gathered from staff and students in three of the demonstration centres Findings showed that the terms 'mentorship', 'assessor' and 'supervisor' were used interchangeably and covered diverse roles in both clinical and community settings Generally there was an impression that staff were willing to help students learn from their experience but felt unprepared for the 'new nursing students' Several factors emerged which seemed either to promote satisfactory experiences for students or inhibit their learning and enjoyment of the placement These are discussed under the themes 'supernumerary status', 'team spirit', 'theory and practice', 'diploma level practice' and 'organization of nursing teams'     

Calcium metabolism in response to heparin administration

Heparin was administered to kittens, to intact cats, and to cats whose thyroids, or parathyroids, or both thyroids and parathyroids had been removed. Over 2 or more months, the serum calcium levels rose in all animals. This result, occurring both in the animals lacking thyroids and parathyroids and in those still having them, suggests that the calcium mobilizing effect of heparin was a direct one.Mayo Clinic and Mayo Foundation: Section of Orthopedic Research (Dr. Jowsey) and Research Assistant (Dr. Adams). Mayo Graduate School of Medicine (University of Minnesota), Rochester: Resident in Orthopedic Surgery (Dr. Schlein). This investigation was supported in part by Research Grant AM-8658 from the National Institutes of Health, Public Health Service. Dr. Adams was the recipient of Research Travel Awards from the Wellcome Trust, London, and The Morgan-Williams Bequest, Welsh National School of Medicine, Cardiff, Wales.     

Stage matters: choosing relevant model systems to address hypotheses in diet and cancer chemoprevention research

Clinical evidence reveals that the efficacy of dietary factors to prevent cancer is probably stage-dependent. The ability to demonstrate stage-specific effects of dietary compounds on normal, preneoplastic and malignant cell models may provide insights into puzzling clinical results from cancer chemoprevention trials. The relevance of these models to the field of cancer prevention is immense and will undoubtedly facilitate the ability to discover which dietary factors are most effective at preventing cancer and which, if any, specific steps in neoplastic transformation render cells refractory to the effects of dietary compounds. There are illustrative examples where exposure of high-risk individuals to dietary chemopreventive agents increases rather than decreases cancer risk. While geneticists and clinical oncologists acknowledge the morphological continuum along which tumors develop in specific tissues, tumor cells, rather than normal and preneoplastic cells, continue to be the primary in vitro reductionist tool employed to elucidate mechanisms underlying disease progression and to investigate the potential utility of dietary as well as other chemopreventive agents. Currently, there are few relevant model systems to study the progression of neoplastic transformation, especially in epithelial cells. We highlight examples of model systems isolated from prostate, breast, endometrial and intestinal tissue, with special emphasis on a specific set of non-tumorigenic, conditionally immortal cell lines derived from C57/BL6 mice [YAMC (Young Adult Mouse Colon cells; Apc+/+) cells and IMCE (Immorto-Min Colonic Epithelium cells; ApcMin/+) cells] that have yielded important information on early events in colorectal neoplasia development. These cell lines are an illustrative example of how researchers can examine stage-dependent effects of specific dietary components on carcinogenesis. The utilization of cell culture systems modeling early, middle and late stages of tumorigenesis will yield important insights into mechanisms by which dietary components impact cancer progression.     

Interleukin-6 production induced by leptin treatment promotes cell proliferation in an Apc (Min/+) colon epithelial cell line

Increased visceral adipose tissue results in elevated plasma leptin, which are associated with increased risk of a number of obesity-related cancers. However, research is contradictory regarding the role of elevated plasma leptin in colon cancer risk. Having established that leptin induced proliferation in a murine model of preneoplastic (Apc(Min/+); IMCE) colon epithelial cells but not normal (Apc(+/+); YAMC) cells, we hypothesized that the leptin-associated IMCE cell proliferation was a result of autocrine interleukin-6 (IL-6) production and ensuing IL-6 receptor (IL-6R) signaling. Here we show, for the first time, that leptin induces elevated IL-6 production in IMCE cells but not in YAMC cells. IL-6 treatment induced cell proliferation in IMCE cells, but not in YAMC cells, in a concentration-dependent manner from 0.1 to 100 ng/ml (P < 0.05). Interleukin-6-induced IMCE cell proliferation was blocked by the addition of a neutralizing anti-IL-6R antibody. In addition, leptin-induced IMCE cell proliferation was blocked by the addition of an anti-IL-6R neutralizing antibody. Further, we elucidate a novel mechanism by which leptin activates TACE/ADAM17-associated IL-6R shedding and trans-IL-6 signaling in IMCE by induction of IL-6 production. IL-6 treatment of IMCE cells was associated with STAT3, ERK, p38, MEK and JAK2 activation and associated STAT3 nuclear activation and translocation. These data implicate leptin-induced IL-6 production, signaling and subsequent STAT3 activation as early events promoting the survival/proliferation of colon epithelial preneoplastic cells. The elucidation of the leptin-initiated mechanism of preneoplastic cell proliferation establishes a biologically plausible link between the adipocyte-specific cytokine leptin and obesity-associated colon cancer.     

Quantitative measurement of fractional bone volume using digital scanning videodensitometry

Summary A method is described for reproducible and rapid quantitative measurements of fractional bone volume in sections of a bone biopsy. The presence or absence of bone is determined at several thousand points over the entire surface area of each specimen by highspeed digitization and computer analysis of video scans of enlarged microradiographic images of bone sections. An operator interactive light-pen assembly permits selective delineation of desired areas of the video image to facilitate computation of regional bone mass within each specimen. Tests of the reproducibility of the method were performed and are described. The results obtained from application of the method to determine the amount of bone in various age groups and in two groups of patients before and after therapy are also presented. These data indicate the potential of this technique for high volume, high resolution measurements of the fractional bone volume in both investigative and clinical diagnostic studies of age dependent and disease dependent processes.     

Borrelia burgdorferi, an extracellular pathogen, circumvents osteopontin in inducing an inflammatory cytokine response

A classic proinflammatory T helper cell type 1 (TH1) response directed against intracellular pathogens includes the cytokine osteopontin, which acts predominantly on macrophages, where it induces the secretion of interleukin (IL)-12 and suppresses the secretion of IL-10. As cell-mediated immune responses play an important role in the resistance to Lyme arthritis, a manifestation of infection by the extracellular pathogen Borrelia burgdorferi, we tested the hypothesis that osteopontin may be required to induce T(H)1 responses and inflammation. The role of osteopontin was tested in vivo and using ex vivo macrophages in B6129F3 mice susceptible to experimental Lyme arthritis. Mice of this genetic background and those fully backcrossed to C57BL/6, which lacked osteopontin expression (spp1-/-), were as susceptible to B. burgdorferi-induced arthritis as littermate controls. Furthermore, equal numbers of spirochetes, as measured by quantitative polymerase chain reaction of the B. burgdorferi gene recA in spp1-/- and B6129F3 wild-type littermates, suggested that susceptibility to infection was not dependent on this cytokine. Neither of the B6129F3 parental mouse strains lacked the ability to secrete osteopontin. spp1-/- mice and controls had immunoglobulin G2 titers, suggestive of a TH1 response. B. burgdorferi was able to directly stimulate the secretion of the proinflammatory cytokines IL-12 and tumor necrosis factor alpha from wild-type and spp1-/- macrophages alike. These results indicate that the usually critical role of osteopontin in the induction of cellular immune responses to intracellular pathogens was circumvented by the ability of the extracellular pathogen B. burgdorferi to induce macrophages directly to produce proinflammatory cytokines.     

NHS cadet schemes: do they widen access to professional healthcare education?

AIM: The aim of this paper is to report a study investigating the extent to which National Health Service cadet schemes widen access to professional health care education. BACKGROUND: Cadet schemes have been reintroduced in the United Kingdom to increase recruitment of nurses and other health care staff to the National Health Service and also to widen access and increase participation in professional health care education by groups poorly represented in such education, including minority ethnic groups. METHODS: A questionnaire survey of all cadet schemes (n = 62) in England at the time of the study was carried out, and the respondents were cadet scheme leaders (n = 62) and cadet students (n = 411). The questionnaires to scheme leaders enquired about when the schemes were established, what the schemes were preparing cadets for, modes of delivery and entry qualifications. The questionnaires to cadets enquired about age, gender, family circumstances, prior experience and ethnic background. FINDINGS: The majority of schemes had been established since the health service reforms of 1999 and most were preparing cadets to enter professional nurse education programmes. Very few provided opportunities for part-time study and some asked for entry qualifications. Cadets were younger on entry than a comparator group of student nurses, fewer were married, fewer had previous employment or health-related employment and a lower percentage of cadets were white. CONCLUSION: Cadet schemes have the potential to widen access to professional health care study, but there is only limited evidence that they are doing so. In particular there was a lack of mature entrants to health care professional education via the schemes. However, the majority of schemes offered a route into professional education for students who did not hold sufficient educational qualifications for direct entry to professional health care education. It is encouraging that cadet schemes appear to be attracting a significantly greater proportion of students from Black and minority ethnic groups than preregistration nursing programmes overall.