Care and services partnership in Quebec birthing centres: myth or reality?

CONTEXT: Working with women to best meet their needs has always been central to midwifery in Quebec, Canada. The creation of birthing centres at the end of the 1990s consolidated this desire to prioritize women's involvement in perinatal care and was intended to encourage the establishment of a care and services partnership between care providers and users. The aim of this pilot study is to evaluate the perceptions of clients, midwives and birth assistants of the way in which women are involved in partnership working in Quebec birthing centres. METHODS: A single qualitative case and pilot study was conducted with midwives (n = 5), birth assistants (n = 4), a manager (n = 1), clients (n = 5) and members of the users' committee (n = 2) at a birthing centre in Quebec, Canada in July and August 2023. The partnership was evaluated using the dimensions of a validated CADICEE questionnaire. RESULTS: The women and professionals stressed that the relationship was established in a climate of trust. The caregivers also attached importance to autonomy, information sharing and decision-making, adaptation to context, empathy and recognition of the couple's expertise. The women confirmed that they establish a relationship of trust with the professionals when the latter show empathy and that they adapt the follow-up to their knowledge and life context. Key factors in establishing this kind of care relationship are the time given, a de-medicalized environment, the comprehensive care received, and professionals who are well-informed about the partnership. In addition, the birthing centre has a users' committee that can put forward ideas but has no decision-making powers. CONCLUSIONS: Both the women and the professionals at the birthing centre appear to be working in partnership. However, at the organizational level, the women are not involved in decision-making. A study of all birthing centres in Quebec would provide a more comprehensive picture of the situation.

Dietary exposure to acrylamide in adolescents from a Canadian urban center.

The distribution of acrylamide in food items frequently consumed by Canadian adolescents was determined along with estimates of their contribution to the overall dietary intake of acrylamide. A total of 196 non-smoking adolescents (10-17 years old) were recruited in Montreal Island population, Canada. Participants were invited to fill out a 2-day food diary and a food frequency questionnaire over the last month. 146 samples of foods most frequently consumed by participants were analyzed for acrylamide contents. The highest acrylamide contents were measured in deep-fried french fries and potato chips (mean ± SD: 1053 ± 657 and 524 ± 276 ng/g respectively). On the basis of the 2-day food diary, median total daily intake of acrylamide was estimated at 0.29 µg/kg bw/d, as compared to 0.17 µg/kg bw/d on the basis of the food frequency questionnaire. These values are similar to those reported in comparable populations. Deep-fried french fries consumption contributed the most to daily acrylamide intake (50%) followed by potato chips (10%), oven-baked french fries (8%) and breakfast cereals (8%). Margins of exposure based on genotoxic benchmark dose limits were estimated to be low (≈<100) in high-consumer adolescents, indicating the need to continue efforts to reduce dietary acrylamide exposure.

Alzheimer type II astrocytic changes following sub-acute exposure to manganese and its prevention by antioxidant treatment.

Exposure to manganese in an industrial or clinical setting can lead to manganism, a neurological disorder with similarities to Parkinson's disease. Although the pathogenetic basis of this disorder is unclear, studies indicate this metal is highly accumulated in astrocytes, suggesting an involvement of these glial cells. To investigate this issue, we have used a recently characterized, sub-acute model of manganese neurotoxicity. Treatment of rats with manganese (II) chloride (50 mg/kg body weight, i.p.) once daily for 1 or 4 days led to increases in manganese levels of up to 232, 523, and 427% in the cerebral cortex, globus pallidus, and cerebellum, respectively, by instrumental neutron activation analysis. These changes were accompanied by development of pathological changes in glial morphology identified as Alzheimer type II astrocytosis in both cortical and sub-cortical structures. Co-treatment with either the antioxidant N-acetylcysteine or the manganese chelator 1,2-cyclohexylenedinitrilotetraacetic acid completely blocked this pathology, indicating the cellular transformation may be mediated by oxidative stress associated with the presence of this metal. These findings represent, to our knowledge, the first report of early induction of this pathological hallmark of manganese neurotoxicity, an event previously considered a consequence of chronic exposure to manganese in primates and in human cases of manganism. Our results also indicate that use of this rodent model may provide a novel opportunity to examine the nature and role of the Alzheimer type II astrocyte in the pathophysiology of this disorder as well as in other disease processes in which cerebral accumulation of manganese occurs.