Food-related parenting practices and styles in households with sibling children: A scoping review.

Interventions that promote responsive feeding in early childhood have been shown to reduce obesity risks. However, interventions mostly target parent-child dyads without considering the complexities of implementing responsive feeding across multiple children within a family unit. This scoping review aims to assess the extent and nature of current literature examining feeding in the context of siblings. Six electronic databases were searched (APA PsycINFO, CINAHL, Embase, Medline, ProQuest Dissertations & Theses Global, and Scopus) for articles published up until November 25, 2021. Studies were included if they compared the use of parent feeding practices and/or styles for two or more siblings aged ≤18 years. Data were extracted from relevant studies and analysed using basic descriptive statistics. A total of 18 studies from North America (n = 12) and Europe (n = 6) were included, with the majority targeting children between 6 and 18 years of age (n = 12). All studies were cross-sectional, with most designed to test differences in parent-reported feeding practices for siblings, primarily restriction and/or pressure to eat, in relation to differences in their characteristics (n = 12). The studies provide some evidence that parents may modify certain feeding practices or styles for siblings in response to differences in their characteristics, such as weight status and eating behaviours. Future research should examine processes that underlie feeding decisions in the context of siblings, including the contexts and consequences of differential feeding, with particular focus on early childhood when feeding interventions may be most effective.

Progress and prospects in treating postmenopausal vaginal atrophy.

Anatomically described as a "potential space," the vagina is a highly estrogen-responsive organ, and its biology changes dramatically at menopause. After menopause, many women experience vaginal dryness and/or dyspareunia, which are caused primarily by regression of the vaginal epithelium.Unlike vasomotor symptoms, which typically resolve overtime, vaginal atrophy remains a persistent consequence of the menopausal transition. This article discusses current trends and potential future treatments that may improve choices for menopausal and postmenopausal women.

Preclinical characterization of selective estrogen receptor beta agonists: new insights into their therapeutic potential.

It has now been over 10 years since Jan-Ake Gustafsson revealed the existence of a second form of the estrogen receptor (ERbeta) at a 1996 Keystone Symposium. Since then, substantial success has been made in distinguishing its potential biological functions from the previously known form (now called ERalpha) and how it might be exploited as a drug target. Subtype selective agonists have been particularly useful in this regard and suggest that ERbeta agonists may be useful for a variety of clinical applications without triggering classic estrogenic side effects such as uterine stimulation. These applications include inflammatory bowel disease, rheumatoid arthritis, endometriosis, and sepsis. This manuscript will summarize illustrative data for three ERbeta selective agonists, ERB-041, WAY-202196, and WAY-200070.

Synthesis and estrogenic activities of novel 7-thiosubstituted estratriene derivatives.

A diastereomerically pure series of 7alpha-thioestratrienes was prepared and evaluated for its affinity for both the human estrogen receptor alpha and the more recently discovered estrogen receptor beta. The functional estrogenic activities of the compounds were measured in a MCF-7 ERE-tk-luciferase assay. The activities and selectivities of the compounds were sensitive to the nature of the thioether side chain.

Suppression of ligand-dependent estrogen receptor activity by bone-resorbing cytokines in human osteoblasts.

Estrogens are important for bone homeostasis and are classified as antiresorptive agents. One of the mechanisms for this effect is the inhibition of cytokine-induced bone resorption, which is mediated in part through an interaction between the estrogen receptor (ER) and nuclear factor (NF)-kappaB in osteoblasts. We present evidence that bone-resorbing cytokines that activate NF-kappaB conversely inhibit ligand-dependent ER activity in the conditionally immortalized human osteoblast cell line, HOB-03-CE6. Treatment of HOB-03-CE6 cells with 17beta-estradiol (17beta-E2) up-regulated reporter gene activity [ERE-thymidine kinase (tk)-luciferase] 3- to 5-fold in a dose-dependent manner (EC50 = 1.0 pM). However, cotreatment of the cells with 17beta-E2 and increasing concentrations of either tumor necrosis factor-alpha (TNF alpha), interleukin-1alpha (IL-1alpha), or IL-1beta completely suppressed ERE-tk-luciferase activity in a dose-dependent manner (IC50 = 0.05-5.0 pM). On the other hand, treatment of the cells with growth factors either up-regulated or had no effect on ERE-tk-luciferase expression. Neither TNF alpha, IL-1alpha, nor IL-1beta treatment affected basal reporter gene activity in the cells, and the TNF alpha effect was reversed by a neutralizing antibody to the cytokine. TNF alpha treatment also suppressed ligand-dependent ER activity in MCF-7 human breast cancer cells, but not in Chinese hamster ovary cells that overexpressed human ER alpha, even though both cell lines responded to the cytokine as measured by the up-regulation of NFkappaB-tk-luciferase activity. TNF alpha treatment did not affect the steady state levels of either ER alpha or ER beta messenger RNA expression by the HOB-03-CE6 cells, nor did it reduce [125I]17beta-E2 binding. Moreover, TNF alpha treatment only weakly inhibited ligand-dependent glucocorticoid receptor activity in the HOB-03-CE6 cells. Bone-resorbing cytokines, which do not signal through the NF-kappaB pathway, did not suppress ERE-tk-luciferase activity in HOB-03-CE6 cells. Treatment of the cells with 17beta-E2 partially suppressed the activation of NF-kappaB by TNF alpha, but did not block cytokine-induced IL-6 secretion. Finally, cotreatment of HOB-03-CE6 cells with an antisense oligonucleotide to NF-kappaB p50 partially reversed the suppression of ERE-tk-luciferase activity by TNF alpha. In summary, these data provide evidence for a potent feedback inhibition of estrogen action in human osteoblasts that is at least partly mediated by the activation of NF-kappaB.

Is curettage needed for uncomplicated incomplete spontaneous abortion?

Spontaneous abortion occurs in 15% to 20% of all human pregnancies. Since the late 1800s, the management of incomplete spontaneous abortion has focused on using curettage to empty the uterus as quickly as possible. This practice began to reduce blood loss and infection and has been unquestioned for 4 decades. In today's medical climate, few spontaneous abortions are the resuslt of illegal manipulation, given the availability of legal pregnancy termination. Antibiotics and transfusions are available, should complications arise in conservatively managed cases. Two prospective randomized trials suggest that conservative management may be advantageous for women who have stable vital signs without evidence of infection. They will have fewer perforations and, possibly, fewer infections and uterine synechiae with expectant or medical management. Larger trials should be undertaken to critically assess surgical evacuation compared to medical management, factoring in the psychologic impact of treatment. We believe that medical management will prove to be the most appropriate treatment for uncomplicated spontaneous incomplete abortion in the 21st century.

Expression of meltrin-alpha mRNA is not restricted to fusagenic cells.

Meltrin-alpha is a myoblast gene product reported to be required for cell fusion [Yagami-Hiromasa et al. (1995): Nature 377:652-656]. Because Northern blots revealed expression only in muscle and bone, the suggestion was made that meltrin-alpha is expressed exclusively by fusagenic cells in these tissues (myoblast and osteoclast). We studied expression of meltrin-alpha mRNA in a panel of tissues and cell lines using the polymerase chain reaction and found it widely expressed. Meltrin-alpha mRNA was readily detected in the osteoblast, the most abundant cell type in bone. In situ hybridization analysis on sections of neonatal mice revealed high levels of expression in the trabecular meshwork of long bones, the basal regions of the dermis and its underlying mesenchyme. We conclude that expression of meltrin-alpha mRNA is not restricted to fusagenic cells and that, in bone, the osteoblast is the major source.

Functional properties of a conditionally phenotypic, estrogen-responsive, human osteoblast cell line.

Osteoblasts are established targets of estrogen action in bone. We screened 66 conditionally immortalized clonal human osteoblast cell lines for estrogen receptors (ERs) using reverse transcriptase-polymerase chain reaction (RT-PCR) analysis for ER alpha mRNA and transactivation of adenovirus-estrogen response element (ERE)-tk-luciferase by 17 beta-estradiol (17 beta-E2) for functional ER protein. One of these cell lines, termed HOB-03-CE6, was chosen for further characterization. The cells, which were conditionally immortalized with a temperature-sensitive SV40 large T antigen, proliferated at the permissive temperature (34 degrees C) but stopped dividing at the nonpermissive temperature (> or = 39 degrees C). Alkaline phosphatase activity and osteocalcin secretion were upregulated by 1 alpha, 25-dihydroxyvitamin D3 in a dose-dependent manner. The cells also expressed type I collagen and other bone matrix proteins, secreted a variety of growth factors and cytokines, formed mineralized nodules based on alizarin red-S and von Kossa histochemical staining, and responded to dexamethasone, all-trans retinoic acid, and transforming growth factor-beta 1. This cell line expressed 42-fold less ER message than MCF-7 human breast cancer cells, as determined by quantitative RT-PCR. However, adenovirus-ERE-tk-luciferase activity was upregulated three- to fivefold in these cells by 17 beta-E2 with an EC50 of 64 pM. Furthermore, this upregulation was suppressed by co-treatment with the anti-estrogen ICI-182, 780. Cytosolic extracts of these cells specifically bound [125I]-17 beta-E2 in a concentration-dependent manner with a Bmax of 2.7 fmoles/mg protein (approximately 1,200 ERs/cell) and a Kd of 0.2 nM. DNA gel-shift analysis using a [32P]-ERE demonstrated the presence of ERs in nuclear extracts of these cells. Moreover, binding of the extracts to this ERE was blocked by a monoclonal antibody to the human ER DNA-binding domain. We evaluated these cells for 14 of 20 reported endogenous responses to 17 beta-E2 in osteoblasts. Although most of these responses appeared to be unaffected by the steroid, 17 beta-E2 suppressed parathyroid hormone-induced cAMP production, as well as basal interleukin-6 mRNA expression; conversely, the steroid upregulated the steady-state expression of alkaline phosphatase message in these cells. In summary, we have identified a clonal, conditionally phenotypic, human osteoblast cell line that expresses functional ERs and exhibits endogenous responses to 17 beta-E2. This cell line will be a valuable in vitro model for exploring some of the molecular mechanisms of estrogen action in bone.