Maternal satisfaction with group care: a systematic review.

OBJECTIVE: This review examined the quantitative relationship between group care and overall maternal satisfaction compared with standard individual care. DATA SOURCES: We searched CINAHL, Clinical Trials, The Cochrane Library, PubMed, Scopus, and Web of Science databases from the beginning of 2003 through June 2023. STUDY ELIGIBILITY CRITERIA: We included studies that reported the association between overall maternal satisfaction and centering-based perinatal care where the control group was standard individual care. We included randomized and observational designs. METHODS: Screening and independent data extraction were carried out by 4 researchers. We extracted data on study characteristics, population, design, intervention characteristics, satisfaction measurement, and outcome. Quality assessment was performed using the Cochrane tools for Clinical Trials (RoB2) and observational studies (ROBINS-I). We summarized the study, intervention, and satisfaction measurement characteristics. We presented the effect estimates of each study descriptively using a forest plot without performing an overall meta-analysis. Meta-analysis could not be performed because of variations in study designs and methods used to measure satisfaction. We presented studies reporting mean values and odds ratios in 2 separate plots. The presentation of studies in forest plots was organized by type of study design. RESULTS: A total of 7685 women participated in the studies included in the review. We found that most studies (ie, 17/20) report higher satisfaction with group care than standard individual care. Some of the noted results are lower satisfaction with group care in both studies in Sweden and 1 of the 2 studies from Canada. Higher satisfaction was present in 14 of 15 studies reporting CenteringPregnancy, Group Antenatal Care (1 study), and Adapted CenteringPregnancy (1 study). Although indicative of higher maternal satisfaction, the results are often based on statistically insignificant effect estimates with wide confidence intervals derived from small sample sizes. CONCLUSION: The evidence confirms higher maternal satisfaction with group care than with standard care. This likely reflects group care methodology, which combines clinical assessment, facilitated health promotion discussion, and community-building opportunities. This evidence will be helpful for the implementation of group care globally.

Endocrine-disrupting chemicals and breastfeeding duration: a review.

PURPOSE OF REVIEW: The purpose of this review is to describe epidemiologic and toxicological literature investigating how endocrine-disrupting chemicals (EDCs) affect mammary gland development and function, thereby impacting lactation duration. RECENT FINDINGS: Perfluoroalkyl and polyfluoroalkyl substances appear to reduce breastfeeding duration through impaired mammary gland development, lactogenesis, and suppressed endocrine signaling. Halogenated aromatic hydrocarbons have differing associations with lactation duration, likely because of the variety of signaling pathways that they affect, pointing to the importance of complex mixtures in epidemiologic studies. Although epidemiologic literature suggests that pesticides and fungicides decrease or have no effect on lactation duration, toxicology literature suggests enhanced mammary gland development through estrogenic and/or antiandrogenic pathways. Toxicological studies suggest that phthalates may affect mammary gland development via estrogenic pathways but no association with lactation duration has been observed. Bisphenol A was associated with decreased duration of breastfeeding, likely through direct and indirect action on estrogenic pathways. SUMMARY: EDCs play a role in mammary gland development, function, and lactogenesis, which can affect breastfeeding duration. Further research should explore direct mechanisms of EDCs on lactation, the significance of toxicant mixtures, and transgenerational effects of EDCs on lactation.

Nickel-Induced Developmental Neurotoxicity in C. elegans Includes Cholinergic, Dopaminergic and GABAergic Degeneration, Altered Behaviour, and Increased SKN-1 Activity.

Nickel (Ni) is a ubiquitous metal in the environment with increasing industrial application. While environmental and occupational exposure to Ni compounds has been known to result in toxicities to several organs, including the liver, kidney, lungs, skin and gonads, neurotoxic effects have not been extensively investigated. In this present study, we investigated specific neuronal susceptibility in a C. elegans model of acute Ni neurotoxicity. Wild-type worms and worms expressing green fluorescent protein (GFP) in either cholinergic, dopaminergic or GABAergic neurons were treated with NiCl2 for 1 h at the first larval (L1) stage. The median lethal dose (LD50) was calculated to be 5.88 mM in this paradigm. Morphology studies of GFP-expressing worms showed significantly increasing degeneration of cholinergic, dopaminergic and GABAergic neurons with increasing Ni concentration. Significant functional changes in locomotion and basal slowing response assays reflected that cholinergic and dopaminergic neuronal function, respectively, were impaired due to Ni treatment. Interestingly, a small but significant number of worms exhibited shrinker phenotype upon Ni exposure but no loopy head foraging behaviour was observed suggesting that function of D-type GABAergic neurons of C elegans may be specifically attenuated while the RME subset of GABAergic neurons are not. GFP expression due to induction of glutathione S-transferase 4 (gst-4), a target of Nrf2 homolog skn-1, was increased in a Pgst-4::GFP worm highlighting Ni-induced oxidative stress. RT-qPCR verified upregulation of this expression of gst-4 immediately after exposure. These data suggest that oxidative stress is associated with neuronal damage and altered behaviour due to developmental Ni exposure.

Iron and manganese-related CNS toxicity: mechanisms, diagnosis and treatment.

INTRODUCTION: Iron (Fe) and manganese (Mn) are essential nutrients for humans. They act as cofactors for a variety of enzymes. In the central nervous system (CNS), these two metals are involved in diverse neurological activities. Dyshomeostasis may interfere with the critical enzymatic activities, hence altering the neurophysiological status and resulting in neurological diseases. Areas covered: In this review, the authors cover the molecular mechanisms of Fe/Mn-induced toxicity and neurological diseases, as well as the diagnosis and potential treatment. Given that both Fe and Mn are abundant in the earth crust, nutritional deficiency is rare. In this review the authors focus on the neurological disorders associated with Mn and Fe overload. Expert commentary: Oxidative stress and mitochondrial dysfunction are the primary molecular mechanism that mediates Fe/Mn-induced neurotoxicity. Although increased Fe or Mn concentrations have been found in brain of patients, it remains controversial whether the elevated metal amounts are the primary cause or secondary consequence of neurological diseases. Currently, treatments are far from satisfactory, although chelation therapy can significantly decrease brain Fe and Mn levels. Studies to determine the primary cause and establish the molecular mechanism of toxicity may help to adapt more comprehensive and satisfactory treatments in the future.