Occupational Performance Coaching for parents of picky eaters: A mixed methods study.

BACKGROUND/AIM: Picky eating is a common childhood phenomenon that impacts many families' occupations surrounding mealtimes. Evidence of the effectiveness of Occupational Performance Coaching (OPC) for caregivers of children suggests it may represent a useful occupation-focused intervention for parents of picky eaters. Using an OPC-targeted intervention, this study aims to report preliminary effectiveness, explore the experience of parents' participation, and investigate factors that influence the OPC intervention. METHODS: This study used an explanatory mixed-method design. Parent participants (n = 8) were recruited via purposive sampling and engaged in three sessions of OPC delivered via an online platform between October and December 2022. Standardised assessments were completed before and after OPC and a qualitative semi-structured interview two weeks after the final OPC session. Variables were analysed descriptively, and independent t tests were performed to compare scores on each standardised assessment pre- and post-intervention. Pearson's correlation analyses were conducted to consider associations between resistance to change and the extent of change in each outcome measure. Reflexive thematic analysis was conducted on postintervention interview transcripts. CONSUMER AND COMMUNITY INVOLVEMENT: Consumer invovlement was limited to parents feedback on their experiences of the intervention. RESULTS: Improvements in occupational performance as measured by the COPM change score were statistically significant (p = <0.001). Child eating behaviours, as measured by the CEBQ Food Fussiness subscale change score (p = 0.01) and BPFAS change score (p = 0.02), demonstrated significant improvements. The extent to which parents viewed these behaviours as problematic as measured by the BPFAS problem change score, showed a significant reduction (p = <0.001). Three themes emerged from interviews with parents: small changes beyond nutrition, parents supported as the experts, and what parents value within an intervention. CONCLUSION: Targeted OPC intervention delivered online by an occupational therapist may be an effective intervention for parents of picky eaters. Future studies using randomised controls are required before OPC can be routinely recommended in a clinical setting for the management of picky eating in children.

A qualitative inquiry of parents of extremely picky eaters: Experiences, strategies and future directions.

BACKGROUND/AIM: Picky eating is a common childhood phenomenon in younger children, impacting family relationships and mealtimes. Limited qualitative studies have explored parents' experiences of parenting an extremely picky eater. This study aimed to address this gap. METHODS: This exploratory qualitative research design included participants who were Australian-based parents (n = 10) of children aged 2-6 years with a minimum picky eating score of 3.33, indicating extreme picky eating, on the Food Fussiness subscale of the Child Eating Behavior Questionnaire (CEBQ). Parents were interviewed online via Zoom using semi-structured interviews focused on their experiences of having a child who is a picky eater. Reflexive thematic analysis was used to analyze the data. RESULTS: Five themes were identified: 1: The picky eating journey for parents. 2: Picky eating impacts families and mealtimes. 3: Parents have attempted multiple strategies to manage picky eating. 4: Emotions associated with parenting an extremely picky eater. 5: Parents of extremely picky eaters have a positive outlook for the future. CONCLUSION: This qualitative study demonstrates that parents' experiences of parenting an extremely picky eater are varied. Parents desire health professionals who listen to their concerns and provide evidence-based knowledge around parent feeding practices to positively impact picky eating.

Picky eating in children: Current clinical trends, practices, and observations within the Australian health-care context.

BACKGROUND/AIM: Childhood picky eating occurs when there is limited intake or variety of food and/or unwillingness to try new foods. Within research settings, standardised assessments are used to describe picky eating behaviours in children. However, little is known about assessment practices of occupational therapists. Similarly, occupational therapy interventions for picky eating in the literature focus on; providing strategies for parents, and working with the child on self-feeding skills. Despite this, interventions and strategies utilised by occupational therapists in clinical practice within an Australian health-care context are unknown. This study examines Australian health professionals' observations of picky eating behaviours, the use of childhood picky eating assessments and interventions, and differences between occupational therapists and other professionals. METHODS: Health professionals (n = 179) were recruited through professional organisations, such as Occupational Therapy Australia. Participants completed an online survey between March and May 2021. Independent variables were reported using descriptive statistics, with logistic regression used to consider differences between occupational therapists and other health professionals. Conventional content analysis was used to analyse responses to open-ended questions. RESULTS: The final sample included 109 eligible participants, with an average of 8.5 years working with picky eaters. Results indicated picky eating behaviours aligned with those reported in the literature. Participants relied on clinical observations and workplace designed assessments. The most common interventions were education, coaching, and the sequential oral sensory approach to feeding. Occupational therapy participants were significantly more likely than other health professional participants to report always using coaching and education. CONCLUSION: Although few health professionals used standardised or validated assessments, the use of education and coaching by occupational therapists aligned with the literature. Results highlight the need for more rigorous investigation to determine the sensitivity of current assessments to differentiate between clinical and typical picky eating, and the effectiveness of interventions for childhood picky eating.

The Link between Suicidality and Electroencephalography Asymmetry: A Systematic Review and Meta-analysis.

As one of the leading causes of death globally, suicide has been researched extensively to better understand factors that confer risk or resilience for suicidality. Promising areas of the literature have focused on brain-based factors that might indicate susceptibility to suicide. Some studies have investigated the link between electroencephalography (EEG) asymmetry, referring to differences in electrical activity in the brain from the left to right hemisphere, and suicidality. The present study is a comprehensive review and meta-analysis of the literature to see if certain patterns in EEG asymmetry serve as a diathesis for suicidal thoughts and behaviors. The results of the current investigation found that EEG asymmetry was not systematically related to suicide based on the literature reviewed. While the present review does not rule out all brain-based factors, the findings suggest that EEG asymmetry may not be a biomarker for suicidality.

Changes in Electroencephalography Alpha Associated With Childhood Neglect and Adolescent Alcohol Use.

The present pilot study is interested in the relationship between childhood neglect, brain function, and alcohol use in adolescence. The goal is to guide future prevention and intervention efforts related to alcohol use following childhood neglect. This pilot study comprised 53 adolescents (12-14 years at baseline) recruited from the Department of Social Services (DSS). Self- and DSS-reported neglect, electroencephalography (EEG) alpha power, and alcohol use behaviors were measured over 1 year. Higher DSS neglect severity in year 1 was related to lower self-efficacy to alcohol use temptation in year 2. Lower EEG alpha power in the parietal region in year 1 was linked to lower self-efficacy to the temptation of alcohol use in year 2. This pilot project has value for using tools, such as EEG, in child maltreatment and alcohol use studies, including with underrepresented adolescents, to better understand brain-related mechanisms in home-based research.

A missense mutation in hepatocyte nuclear factor-4 alpha, resulting in a reduced transactivation activity, in human late-onset non-insulin-dependent diabetes mellitus.

Non-insulin-dependent diabetes mellitus (NIDDM) is a heterogeneous disorder characterized by hyperglycemia resulting from defects in insulin secretion and action. Recent studies have found mutations in the hepatocyte nuclear factor-4 alpha gene (HNF-4alpha) in families with maturity-onset diabetes of the young (MODY), an autosomal dominant form of diabetes characterized by early age at onset and a defect in glucose-stimulated insulin secretion. During the course of our search for susceptibility genes contributing to the more common late-onset NIDDM forms, we observed nominal evidence for linkage between NIDDM and markers in the region of the HNF-4alpha/MODY1 locus in a subset of French families with NIDDM diagnosed before 45 yr of age. Thus, we screened these families for mutations in the HNF-4alpha gene. We found a missense mutation, resulting in a valine-to-isoleucine substitution at codon 393 in a single family. This mutation cosegregated with diabetes and impaired insulin secretion, and was not present in 119 control subjects. Expression studies showed that this conservative substitution is associated with a marked reduction of transactivation activity, a result consistent with this mutation contributing to the insulin secretory defect observed in this family.

Hepatocyte nuclear factor 4 alpha ligand binding and F domains mediate interaction and transcriptional synergy with the pancreatic islet LIM HD transcription factor Isl1.

The orphan nuclear receptor HNF4alpha and the LIM homeodomain factor Isl1 are co-expressed in pancreatic beta-cells and are required for the differentiation and function of these endocrine cells. HNF4alpha activates numerous genes and mutations in its gene are associated with maturity onset diabetes of the young. Cofactors and transcription factors that interact with HNF4alpha are crucial to modulate its transcriptional activity, since the latter is not regulated by conventional ligands. These transcriptional partners interact mainly through the HNF4alpha AF-1 module and the ligand binding domain, which contains the AF-2 module. Here, we showed that Isl1 could enhance the HNF4alpha-mediated activation of transcription of the HNF1alpha, PPARalpha and insulin I promoters. Isl1 interacted with the HNF4alpha AF-2 but also required the HNF4alpha carboxy-terminal F domain for optimal interaction and transcriptional synergy. More specifically, we found that naturally occurring HNF4alpha isoforms, differing only in their F domain, exhibited different abilities to interact and synergize with Isl1, extending the crucial transcriptional modulatory role of the HNF4alpha F domain. HNF4alpha interacted with both the homeodomain and the first LIM domain of Isl1. We found that the transcriptional synergy between HNF4alpha and Isl1 involved an increase in HNF4alpha loading on promoter. The effect was more pronounced on the rat insulin I promoter containing binding sites for both HNF4alpha and Isl1 than on the human HNF1alpha promoter lacking an Isl1 binding site. Moreover, Isl1 could mediate the recruitment of the cofactor CLIM2 resulting in a further transcriptional enhancement of the HNF1alpha promoter activity.

Hepatocyte nuclear factor 4alpha enhances the hepatocyte nuclear factor 1alpha-mediated activation of transcription.

Hepatocyte Nuclear Factor 1alpha (HNF1alpha) and Hepatocyte Nuclear Factor 4alpha (HNF4alpha) are two liver-enriched transcription factors coexpressed in specific tissues where they play a crucial role through their involvement in a complex cross-regulatory network. HNF1alpha down regulates HNF4alpha-mediated activation of transcription via a direct protein-protein interaction. Here we show that HNF4alpha enhances the transcriptional activity of HNF1alpha in a DNA binding independent manner, thus indicating that it behaves as a HNF1alpha coactivator. Using mutations in the ligand binding domain (LBD) of HNF4alpha, we confirmed the involvement of the Activation Function 2 module and demonstrated the requirement of the integrity of the LBD for the interaction with HNF1alpha. Moreover, we show that HNF4alpha cooperates with p300 to achieve the highest HNF1alpha-mediated transcription rates. Our findings highlight a new way by which HNF4alpha can regulate gene expression and extend our knowledge of the complexity of the transcriptional network involving HNF4alpha and HNF1alpha.

Characterization of the chromosomal protein MC1 from the thermophilic archaebacterium Methanosarcina sp. CHTI 55 and its effect on the thermal stability of DNA.

In the deoxyribonucleoprotein complex of Methanosarcina sp. CHTI 55, DNA is associated with two proteins, named MC1 (methanogen chromosomal protein 1) (Mr 10,760) and MC2 (Mr 17,000). Protein MC1, the most abundant of these proteins, is closely related to the Methanosarcina barkeri MS protein MC1. The effect of Methanosarcina sp. CHTI 55 protein MC1 on the thermal stability of DNA has been studied in native deoxyribonucleoprotein complex, as well as in reconstituted complexes, and it has been compared to the effect of E. coli DNA-binding protein II. Both proteins are able to protect DNA against thermal denaturation, but the differences observed in the melting profiles suggest that they interact by different mechanisms. Moreover, our studies indicate that one molecule of protein MC1 protects eight base pairs of DNA.

Isolation and characterization of DNA-binding proteins from the cyanobacterium Synechococcus sp. PCC 7002 (Agmenellum quadruplicatum) and from spinach chloroplasts.

Basic, low-molecular-weight DNA-binding proteins were isolated from the unicellular cyanobacterium Synechococcus sp. PCC 7002 (Agmenellum quadruplicatum) and from the chloroplasts of spinach (Spinacia oleacera). In Synechococcus, two major proteins which bind to double-strand DNA (10 and 16 kDa, respectively) were purified. The 10 kDa protein, named HAq, resembles strongly, in amino-acid composition, eubacterial HU-type proteins. The 16 kDa protein is slightly basic. Its characteristics are compared to those of E. coli protein H1 and 17K. In spinach chloroplasts, a major protein HC (10 kDa), which also binds to ds-DNA, was purified. As observed for known archaebacterial and mitochondrial DNA-binding proteins, its amino-acid composition differs significantly from those of eubacterial HU. The comparison of the amino-terminal sequence (27 residues) with other chloroplast peptidic sequences is discussed.

Primary structure of the chromosomal protein MC1 from the archaebacterium Methanosarcina sp. CHTI 55.

The DNA of the thermophilic archaebacterium Methanosarcina sp. CHTI 55 has been shown to be associated with two proteins called MC1 and MC2, of molecular mass 11 kDa and 17 kDa (Chartier et al. (1988) Biochim. Biophys. Acta 951, 149-156). The most abundant of these proteins, protein MC1, can protect DNA against thermal denaturation. In the present paper we report the covalent structure of protein MC1 and its effect on transcription of DNA in vitro. The covalent structure was determined from automated sequence analysis of the protein and from structural data provided by peptides derived from cleavage of the protein at aspartic acid and arginine residues. The amino-acid sequence of protein MC1 from Methanosarcina sp. CHTI 55 is closely related to that of the protein MC1 (previously called HMb) isolated from Methanosarcina barkeri strain MS: among the nine substitutions observed between the two proteins seven are conservative. Transcription of DNA in vitro is stimulated by protein MC1 at low protein-to-DNA ratio but is inhibited at a ratio higher than 0.1 (w/w), which is the one determined in the bacterial deoxyribonucleoprotein complex.

Conformational study of the chromosomal protein MC1 from the archaebacterium Methanosarcina barkeri.

Methanogen chromosomal protein MC1 is a polypeptide of 93 amino acid residues (Mr 10,757) which represents the major protein associated with the DNA of the archaebacterium Methanosarcina barkeri and can protect DNA against thermal denaturation. The conformation of protein MC1 has been investigated by means of predictive methods, infrared spectroscopy, circular dichroism and tryptophan fluorescence studies. Protein MC1 has a low amount of alpha-helix but contains antiparallel beta-sheet strands. The larger hydrophobic cluster which contains tryptophan at position 61 appears buried in the protein. Addition of salts induces the unfolding of the protein and makes the tryptophan indole ring more rigid. With respect to its primary structure and its conformation, protein MC1 appears radically different from the chromosomal DNA-binding protein II (also called HU-type protein) in eubacteria.

Functional study of the E276Q mutant hepatocyte nuclear factor-4alpha found in type 1 maturity-onset diabetes of the young: impaired synergy with chicken ovalbumin upstream promoter transcription factor II on the hepatocyte nuclear factor-1 promoter.

Seven mutations in the hepatocyte nuclear factor (HNF)-4alpha gene have been shown to correlate with type 1 maturity-onset diabetes of the young (MODY 1), a monogenic form of type 2 diabetes. Up to now, only the functional properties of two MODY 1 HNF-4alpha mutants, Q268X and V393I, have been investigated to address how the mutations in the HNF-4alpha gene, found by genetic studies, can give rise to impaired activities of mutated HNF-4alpha proteins and can cause this disease. The E276Q mutation results in a nonconservative substitution occurring in the HNF-4alpha E domain, which is involved in dimerization and transactivation activities as well as in protein-protein interactions with other transcription factors or coactivators. Using the mutated human HNF-4alpha2, we have found that, in the absence of chicken ovalbumin upstream promoter transcription factor II (COUP TFII), the E276Q substitution does not significantly affect the dimerization and transactivating activities of HNF-4alpha, at least on the promoters studied herein. On the other hand, in the presence of COUP TFII, the substitution impairs the enhancement of HNF-4-mediated activation of HNF-1 promoter. The impaired synergy between COUP TFII and HNF-4 on the HNF-1 promoter results from an alteration of their interaction. HNF-1 expression plays a crucial role in transactivation of insulin promoter and of numerous genes coding for enzymes involved in glucose homeostasis. Therefore, its downregulation resulting from the E276Q mutation in HNF-4alpha gene most probably impairs the function of pancreatic beta-cells.

Maturity-onset diabetes of the young Type 1 (MODY1)-associated mutations R154X and E276Q in hepatocyte nuclear factor 4alpha (HNF4alpha) gene impair recruitment of p300, a key transcriptional co-activator.

Hepatocyte nuclear factor 4alpha (HNF4alpha) is a nuclear receptor involved in glucose homeostasis and is required for normal beta-cell function. Mutations in the HNF4alpha gene are associated with maturity-onset diabetes of the young type 1. E276Q and R154X mutations were previously shown to impair intrinsic transcriptional activity (without exogenously supplied co-activators) of HNF4alpha. Given that transcriptional partners of HNF4alpha modulate its intrinsic transcriptional activity and play crucial roles in HNF4alpha function, we investigated the effects of these mutations on potentiation of HNF4alpha activity by p300, a key co-activator for HNF4alpha. We show here that loss of HNF4alpha function by both mutations is increased through impaired physical interaction and functional cooperation between HNF4alpha and p300. Impairment of p300-mediated potentiation of HNF4alpha transcriptional activity is of particular importance for the E276Q mutant since its intrinsic transcriptional activity is moderately affected. Together with previous results obtained with chicken ovalbumin upstream promoter-transcription factor II, our results highlight that impairment of recruitment of transcriptional partners represents an important mechanism leading to abnormal HNF4alpha function resulting from the MODY1 E276Q mutation. The impaired potentiations of HNF4alpha activity were observed on the promoter of HNF1alpha, a transcription factor involved in a transcriptional network and required for beta-cell function. Given its involvement in a regulatory signaling cascade, loss of HNF4alpha function may cause reduced beta-cell function secondary to defective HNF1alpha expression. Our results also shed light on a better structure-function relationship of HNF4alpha and on p300 sequences involved in the interaction with HNF4alpha.

Hepatocyte nuclear factor 4 alpha isoforms originated from the P1 promoter are expressed in human pancreatic beta-cells and exhibit stronger transcriptional potentials than P2 promoter-driven isoforms.

The nuclear receptor hepatocyte nuclear factor (HNF) 4 alpha is involved in a transcriptional network and plays an important role in pancreatic beta-cells. Mutations in the HNF4 alpha gene are correlated with maturity-onset diabetes of the young 1. HNF4 alpha isoforms result from both alternative splicing and alternate usage of promoters P1 and P2. It has recently been reported that HNF4 alpha transcription is driven almost exclusively by the P2 promoter in pancreatic islets. We observed that transcripts from both P1 and P2 promoters were expressed in human pancreatic beta-cells and in the pancreatic beta-cell lines RIN m5F and HIT-T15. Expression of HNF4 alpha proteins originating from the P1 promoter was confirmed by immunodetection. Due to the presence of the activation function module AF-1, HNF4 alpha isoforms originating from the P1 promoter exhibit stronger transcriptional activities and recruit coactivators more efficiently than isoforms driven by the P2 promoter. Conversely, activities of isoforms produced by both promoters were similarly repressed by the corepressor small heterodimer partner. These behaviors were observed on the promoter of HNF1 alpha that is required for beta-cell function. Our results highlight that expression of P1 promoter-driven isoforms is important in the control of pancreatic beta-cell function.

Cloning and sequencing of cDNAs encoding the human hepatocyte nuclear factor 4 indicate the presence of two isoforms in human liver.

Hepatocyte nuclear factor 4 (HNF-4) is a key transcription factor involved in the specific expression of many genes in liver and intestine. Sequences of cDNAs coding for HNF-4 have been established in rat and Drosophila melanogaster. Rat HNF-4 exhibits two isoforms which probably result from differential splicing. We have isolated HNF-4 cDNAs from an adult human cDNA library. Sequence analysis revealed that two HNF-4 isoforms are also present in human liver. The complete sequence of the longest human isoform has been established and compared to the rat HNF-4 amino-acid sequences.

Purification and characterization of two basic spermatid-specific proteins isolated from the dog-fish Scylliorhinus caniculus.

In dog-fish spermatid nuclei two intermediate proteins S1 and S2 replace histones before the setting down of protamines. These spermatid-specific proteins were isolated by carboxymethyl-cellulose chromatography and purified by high pressure liquid chromatography. S1 and S2 are characterized by a high content of basic residues and by the lack of cysteine and phenylalanine. The determination of their amino acid composition and of their N- and C-terminal sequences prove that each protein corresponds to a specific molecule which can be considered neither as a histone hydrolytic product nor as a protamines precursor.

Stoichiometry of the binding of chromosomal protein MC1 from the archaebacterium, Methanosarcina spp. CHTI55, to DNA.

We have investigated the binding stoichiometry of the chromosomal MC1 protein on DNA using the gel retardation technique. Analysis of the distribution of the complex containing 0, 1, 2, 3 ... bound proteins shows that the protein MC1 interacts with the DNA as a monomer. Binding experiments with short DNA fragments of various lengths shows that the site size is 11 bp in length. These results are compared to those obtained with other chromosomal proteins including HU protein.

Functional properties of the R154X HNF-4alpha protein generated by a mutation associated with maturity-onset diabetes of the young, type 1.

Mutations in the hepatocyte nuclear factor 4alpha (HNF-4alpha) gene are associated with one form of maturity-onset diabetes of the young (MODY1). The R154X mutation generates a protein lacking the E-domain which is required for normal HNF-4alpha functions. Since pancreatic beta-cell dysfunction is a feature of MODY1 patients, we compared the functional properties of the R154X mutant in insulin-secreting pancreatic beta-cells and non-beta-cells. The R154X mutation did not affect nuclear localisation in beta-cells and non-beta-cells. However, it did lead to a greater impairment of HNF-4a function in beta-cells compared to non-beta-cells, including a complete loss of transactivation activity and a dominant-negative behaviour. .

Primary structure of chicken erythrocyte histone H2A.

The complete amino acid sequence (128 residues) of the chicken erythrocyte histone H2A was deduced from the data provided by structural studies on the tryptic peptides from the maleylated histone and of the peptides obtained by thermolysin digestion of the native protein. The sequence of chicken histone H2A differs from the calf homologous histone by the deletion of one residue of histidine at position 123 or 124 and three conservative substitutions: a residue of serine replaces a residue of threonine at position 16, a residue of aspartic acid replaces a residue of glutamic acid at position 121 and a residue of alanine replaces a residue of glycine at position 128.