Miracle-dz/UniFAR-FTUs huggingface dataset:
Feeding strategies used by primary school meal staff and their impact on children's eating.

BACKGROUND In parent-child interactions, feeding strategies including pressure, restriction, modelling, rewards, encouragement and repeated taste exposure have been reliably shown to influence children's eating. Because there is no evidence that the psychosocial interactions inherent in the strategies are context-dependent, the present study investigated their utilisation during primary school meal supervision. METHODS A case study of one Local Authority in Wales was conducted involving eleven primary schools stratified into socio-economic quartiles. Focussed observations were carried out over two to three lunchtimes per school to explore the feeding strategies, outcomes and behaviours inherent in the dining hall context. These were supplemented by semi-structured interviews with catering staff and midday supervisors, which were carried out after the observation session. RESULTS Most feeding strategies used by school meal staff reflected those reported in the literature (e.g. pressure, encouragement and rewards), although purposeful modelling of eating behaviours was not found and the imposition of food norms, such as eating dessert last, was common. Dining hall staff readily, if not consistently, used these strategies, although the constraints and opportunities of each dining hall context influenced their selection and implementation. However, even if children left the service point with nutritionally balanced meals, they often failed to eat them. CONCLUSIONS Because repeated taste exposure is known to increase liking for foods, further studies are recommended to investigate how the naturally occurring feeding strategies evident in primary school dining halls could be harnessed to encourage children to taste the nutritionally balanced schools meals that school meal transformation programmes will expose them to.
Hyperactivation of Mammalian Target of Rapamycin Complex 1 (mTORC1) Promotes Breast Cancer Progression through Enhancing Glucose Starvation-induced Autophagy and Akt Signaling*

Background: TSC1 is a negative regulator for mTORC1 that is implicated in cancer. Results: mTORC1 activation by TSC1 deletion promotes mammary tumor growth through increasing autophagy and Akt activation of tumor cells. Conclusion: mTORC1 activation in mammary tumor cells is important in promoting breast cancer progression in vivo. Significance: New insights into the mechanisms of breast cancer progression may offer potential targets in breast cancer therapy. The mammalian target of rapamycin complex 1 (mTORC1) is a master regulator of cell growth and proliferation. Recent studies have suggested that constitutive activation of mTORC1 in normal cells could lead to malignant tumor development in several tissues. However, the mechanisms of mTORC1 hyperactivation to promote the growth and metastasis of breast or other cancers are still not well characterized. Here, using a new inducible deletion system, we show that deletion of Tsc1 in mouse primary mammary tumor cells, either before or after their transplantation, significantly increased their growth in vivo. The increase in tumor growth was completely rescued by rapamycin treatment, suggesting a major contribution from mTORC1 hyperactivation. Interestingly, glucose starvation-induced autophagy, but not amino acid starvation-induced autophagy, was increased significantly in Tsc1-null tumor cells. Further analysis of these cells also showed an increased Akt activation but no significant changes in Erk signaling. Together, these results provide insights into the mechanism by which hyperactivation of mTORC1 promotes breast cancer progression through increasing autophagy and Akt activation in vivo.
What clinical characteristics of children with autism influence their inclusion in regular classrooms?

BACKGROUND This study took place in the context of recent legislation enacted in several countries--including France--and aimed at promoting inclusion of children with intellectual disabilities. It focuses on young children with autism and examines the links between the children's characteristics and their weekly hours of regular-classroom inclusion and intervention in specialised setting. METHOD Standardised clinical and sociodemographic data were collected for 77 children with autism, along with data about their interventional programmes. RESULTS The study showed that the number of hours of inclusion at school was influenced by the children's behavioural and adaptive characteristics, as well as by the socioprofessional category of their parents, although these factors did not affect the number of hours spent in specialised setting. Moreover, the total amount of time per week spent in interventional services of any kind was very small for some of the children. CONCLUSION The time spent in special-intervention services and regular classrooms combined did not add up to an adequate number of weekly hours for these children, particularly those exhibiting at least one of the following characteristics: low adaptation level, major behavioural problems or low socioprofessional category of parents.
A Case Study of 1.5 Generation Chinese American Women's Perspectives of Nutrition Education

A CASE STUDY OF 1.5 GENERATION CHINESE AMERICAN WOMEN’S PERSPECTIVES OF NUTRITION EDUCATION Diana F. Karczmarczyk, Ph.D. George Mason University, 2013 Dissertation Chair Dr. Anastasia P. Samaras The purpose of this study is to explore the perspectives of 1.5 generation (defined as immigrants who enter the United States between the ages of 12 and 15) Chinese American women regarding nutrition education. Although much has been written about the importance of delivering culturally competent nutrition education, insufficient attention has been given to the needs and experiences of this generation of Chinese American women. In addition, there is little disaggregated research on the unique needs and perceptions of Asian American subgroups, including those of Chinese Americans, the largest Asian community in the US. This research is focused specifically on 1.5 Chinese American women to provide an in-depth understanding of their perspectives about nutrition. The qualitative case-study research design uses a Three Tier Structure Approach, designed by the researcher and adapted from the Mears’ (2009) Gateway Approach, entailing an open-ended written narrative followed by two interviews organized within a Three Tier Structure Approach. In Tier One, in response to a question on beliefs about nutrition in the US, five participants identified and shared a critical incident through an open-ended written narrative. Of those five participants, three then completed Tier Two and Tier Three, which entailed semi-structured face-to-face interviews to further probe their individual perspectives about their experiences with nutrition education, sources of knowledge, messages in their community, eating and food preparation behaviors, and their perspectives on and recommendations for delivery of nutrition education. Although the participants in this study were demographically similar in terms of current age, age at immigration, and place of birth, their experiences with nutrition education in the US varied. In addition, none of the participants reported receiving formal nutrition education from a health-care professional or nutritionist. Messages participants had received about nutrition education varied and came from family, friends, and the media. This study adds to the resources currently available to health-care providers, and particularly nutrition educators, which can be used in the development and implementation of culturally competent nutrition education interventions for 1.5 generation Chinese American women. Recommendations for both nutrition educators and health-care professionals are identified to help address the needs of this population. Nutrition educators, for example, should offer culturally appropriate nutrition education to 1.5 generation Chinese American women, offer nutrition education consistently, and use a wide variety of outreach approaches to deliver this education. Recommendations for health-care professionals include conducting a quality needs analysis with each patient.
Cause-specific mortality and death certificate reporting in adults with moderate to profound intellectual disability.

BACKGROUND The study of premature deaths in people with intellectual disability (ID) has become the focus of recent policy initiatives in England. This is the first UK population-based study to explore cause-specific mortality in adults with ID compared with the general population. METHODS Cause-specific standardised mortality ratios (SMRs) and exact 95% confidence intervals were calculated by age and sex for adults with moderate to profound ID living in the unitary authorities of Leicester, Leicestershire and Rutland, UK, between 1993 and 2006. Causes of death were also studied to determine how often ID and associated conditions, such as Down syndrome, were mentioned. RESULTS A total of 503 (17% of population) adults with ID died during the 14-year study period (30 144 person-years). Relatively high cause-specific mortality was seen for deaths caused by congenital abnormalities (SMR = 8560), diseases of the nervous system and sense organs (SMR = 1630), mental disorders (other than dementia) (SMR = 1141) and bronchopneumonia (SMR = 647). Excess deaths were also seen for diseases of the genitourinary system or digestive system, cerebrovascular disease, other respiratory infections, dementia (in men only), other circulatory system diseases (in women only) and accidental deaths (in women only). Two-fifths (n = 204; 41%) of deaths recorded in adults with ID mentioned ID or an associated condition as a contributing cause of death. CONCLUSIONS Strategies to reduce inequalities in people with ID need to focus on decreasing mortality from potentially preventable causes, such as respiratory infections, circulatory system diseases and accidental deaths. The lack of mention of ID on death certificates highlights the importance of effective record linkage and ID reporting in health and social care settings to facilitate the government's confidential inquiry into causes of death in this population.
Delay in Apoptosome Formation Attenuates Apoptosis in Mouse Embryonic Stem Cell Differentiation

Background: The mitochondrial apoptotic pathway has a non-apoptotic role in cell differentiation. Results: Differentiation of mouse embryonic stem cells into cardiomyocytes passes through a mitochondrial pathway of apoptosis. Conclusion: The delayed mitochondrial apoptotic pathway in mouse embryonic stem cells delivers cells into differentiation, not cell death. Significance: Such a comparative study could help to clarify ambiguities about the death-centric model of differentiation. Differentiation is an inseparable process of development in multicellular organisms. Mouse embryonic stem cells (mESCs) represent a valuable research tool to conduct in vitro studies of cell differentiation. Apoptosis as a well known cell death mechanism shows some common features with cell differentiation, which has caused a number of ambiguities in the field. The research question here is how cells could differentiate these two processes from each other. We have investigated the role of the mitochondrial apoptotic pathway and cell energy level during differentiation of mESCs into the cardiomyocytes and their apoptosis. p53 expression, cytochrome c release, apoptosome formation, and caspase-3/7 activation are observed upon induction of both apoptosis and differentiation. However, remarkable differences are detected in time of cytochrome c appearance, apoptosome formation, and caspase activity upon induction of both processes. In apoptosis, apoptosome formation and caspase activity were observed rapidly following the cytochrome c release. Unlike apoptosis, the release of cytochrome c upon differentiation took more time, and the maximum caspase activity was also postponed for 24 h. This delay suggests that there is a regulatory mechanism during differentiation of mESCs into cardiomyocytes. The highest ATP content of cells was observed immediately after cytochrome c release 6 h after apoptosis induction and then decreased, but it was gradually increased up to 48 h after differentiation. These observations suggest that a delay in the release of cytochrome c or delay in ATP increase attenuate apoptosome formation, and caspase activation thereby discriminates apoptosis from differentiation in mESCs.
Circadian Control of Fatty Acid Elongation by SIRT1 Protein-mediated Deacetylation of Acetyl-coenzyme A Synthetase 1*

Background: Circadian clock regulates various aspects of metabolism. Results: Rhythmic acetylation of AceCS1 controls circadian oscillations in acetyl-CoA levels and in fatty acid elongation. Conclusion: A previously unrecognized regulation of acetyl-CoA provides additional evidence to circadian regulation of metabolism. Significance: Understanding of the role of acetyl-CoA in fatty acid elongation might provide therapeutic benefits for treating metabolic diseases and cancer. The circadian clock regulates a wide range of physiological and metabolic processes, and its disruption leads to metabolic disorders such as diabetes and obesity. Accumulating evidence reveals that the circadian clock regulates levels of metabolites that, in turn, may regulate the clock. Here we demonstrate that the circadian clock regulates the intracellular levels of acetyl-CoA by modulating the enzymatic activity of acetyl-CoA Synthetase 1 (AceCS1). Acetylation of AceCS1 controls the activity of the enzyme. We show that acetylation of AceCS1 is cyclic and that its rhythmicity requires a functional circadian clock and the NAD+-dependent deacetylase SIRT1. Cyclic acetylation of AceCS1 contributes to the rhythmicity of acetyl-CoA levels both in vivo and in cultured cells. Down-regulation of AceCS1 causes a significant decrease in the cellular acetyl-CoA pool, leading to reduction in circadian changes in fatty acid elongation. Thus, a nontranscriptional, enzymatic loop is governed by the circadian clock to control acetyl-CoA levels and fatty acid synthesis.
A Novel Unsaturated β-Glucuronyl Hydrolase Involved in Ulvan Degradation Unveils the Versatility of Stereochemistry Requirements in Family GH105*

Background: Biodegradation of green algal cell wall requires specialized enzymatic machinery, which is not yet well characterized. Results: Structural and biochemical characterization of a new β-glucuronyl hydrolase belonging to family GH105 active on oligo-ulvans. Conclusion: The GH105 family encompasses enzymes cleaving both α- and β-linked glycosides. Significance: Investigations of enzymatic degradation of marine polysaccharides reveals enzymes with unique characteristics. Ulvans are cell wall matrix polysaccharides in green algae belonging to the genus Ulva. Enzymatic degradation of the polysaccharide by ulvan lyases leads to the production of oligosaccharides with an unsaturated β-glucuronyl residue located at the non-reducing end. Exploration of the genomic environment around the Nonlabens ulvanivorans (previously Percicivirga ulvanivorans) ulvan lyase revealed a gene highly similar to known unsaturated uronyl hydrolases classified in the CAZy glycoside hydrolase family 105. The gene was cloned, the protein was overexpressed in Escherichia coli, and enzymology experiments demonstrated its unsaturated β-glucuronyl activity. Kinetic analysis of purified oligo-ulvans incubated with the new enzyme showed that the full substrate specificity is attained by three subsites that preferentially bind anionic residues (sulfated rhamnose, glucuronic/iduronic acid). The three-dimensional crystal structure of the native enzyme reveals that a trimeric organization is required for substrate binding and recognition at the +2 binding subsite. This novel unsaturated β-glucuronyl hydrolase is part of a previously uncharacterized subgroup of GH105 members and exhibits only a very limited sequence similarity to known unsaturated β-glucuronyl sequences previously found only in family GH88. Clan-O formed by families GH88 and GH105 was singular in the fact that it covered families acting on both axial and equatorial glycosidic linkages, respectively. The overall comparison of active site structures between enzymes from these two families highlights how that within family GH105, and unlike for classical glycoside hydrolysis, the hydrolysis of vinyl ether groups from unsaturated saccharides occurs independently of the α or β configuration of the cleaved linkage.
A Transient Interaction between the Phosphate Binding Loop and Switch I Contributes to the Allosteric Network between Receptor and Nucleotide in Gαi1*

Background: G proteins couple receptor binding to nucleotide release via an allosteric network. Results: Mutation of allosteric sites of Gαi1 stabilizes a transient signaling conformation and may highlight an allosteric connection between receptor and nucleotide. Conclusion: The P-loop interacts with Switch I in the K345L variant of Gαi1. Significance: G protein signaling is critical for numerous cellular functions, and GDP release is the rate-limiting step of the cycle. Receptor-mediated activation of the Gα subunit of heterotrimeric G proteins requires allosteric communication between the receptor binding site and the guanine nucleotide binding site, which are separated by >30 Å. Structural changes in the allosteric network connecting these sites are predicted to be transient in the wild-type Gα subunit, making studies of these connections challenging. In the current work, site-directed mutants that alter the energy barriers between the activation states are used as tools to better understand the transient features of allosteric signaling in the Gα subunit. The observed differences in relative receptor affinity for intact Gαi1 subunits versus C-terminal Gαi1 peptides harboring the K345L mutation are consistent with this mutation modulating the allosteric network in the protein subunit. Measurement of nucleotide exchange rates, affinity for metarhodopsin II, and thermostability suggest that the K345L Gαi1 variant has reduced stability in both the GDP-bound and nucleotide-free states as compared with wild type but similar stability in the GTPγS-bound state. High resolution x-ray crystal structures reveal conformational changes accompanying the destabilization of the GDP-bound state. Of these, the conformation for Switch I was stabilized by an ionic interaction with the phosphate binding loop. Further site-directed mutagenesis suggests that this interaction between Switch I and the phosphate binding loop is important for receptor-mediated nucleotide exchange in the wild-type Gαi1 subunit.
Neuropsychological differences between survivors of supratentorial and infratentorial brain tumours.

BACKGROUND The purpose of this study is to evaluate the relationship between brain tumour location and core areas of cognitive and behavioural functioning for paediatric brain tumour survivors. The extant literature both supports and refutes an association between paediatric brain tumour location and neurocognitive outcomes. We examined neuropsychological test data to identify any differences in neurocognitive and behavioural profile associated with supratentorial versus infratentorial tumour location. METHODS Following Institutional Review Board approval, the medical records and neuropsychological test data collected between 1997 and 2002 for 70 children treated for brain tumour at Children's Hospital Los Angeles were reviewed. Fifty-one per cent of the participants had tumours located in the supratentorial regions of the brain, whereas 49% had infratentorial tumours. Primary medical treatments involved tumour resection (90%), cranial radiation therapy (76%), chemotherapy (71%), and 59% all three medical procedures. The two tumour location groups did not differ significantly in the cumulative treatment dose of irradiation to the tumour bed or in the dose delivered to the whole brain. Neuropsychological test data included measures of verbal and non-verbal intellectual functioning, attention/working memory, processing speed, verbal and visual memory, fine motor skills, visual-motor integration, academic achievement, and social-emotional functioning. Differences between the two groups were evaluated using anova, t-tests and chi-squared statistical tests. RESULTS The supratentorial and infratentorial tumour location groups did not differ on measures of intellectual functioning. However, survivors of infratentorial tumours performed more poorly on selected measures of more specific cognitive functions and on parent-report of social-emotional functioning relative to survivors of supratentorial tumours, even when age at diagnosis was held as a covariate. Higher frequency of auditory deficits was noted in the infratentorial tumour group and was associated with lowered academic achievement scores. CONCLUSIONS The differences by location found in more specific neurocognitive and social-emotional variables, after controlling for age at diagnosis, may possibly reflect tumour location-specific effects. However, this interpretation remains tentative given the limitations in our study and inability to control for the range of medical and treatment-related factors that may have contributed towards the outcomes observed in our sample. At the same time, most of our findings appear consistent with reports from recent studies in this area.
Co-Activation of Nuclear Factor-κB and Myocardin/Serum Response Factor Conveys the Hypertrophy Signal of High Insulin Levels in Cardiac Myoblasts*

Background: Mechanisms of cardiac hypertrophy in states of insulin resistance/high insulin remain poorly understood. Results: In response to high insulin, myocardin/SRF expression in cardiac myoblasts is related to the development of cardiac myoblast hypertrophy. Conclusion: Myocardin acts, with Nuclear Factor-κB, as a nuclear effector of insulin, promoting cardiac hypertrophy. Significance: Understanding these mechanisms may help designing strategies to prevent diabetic cardiomyopathy. Hyperinsulinemia contributes to cardiac hypertrophy and heart failure in patients with the metabolic syndrome and type 2 diabetes. Here, high circulating levels of tumor necrosis factor (TNF)-α may synergize with insulin in signaling inflammation and cardiac hypertrophy. We tested whether high insulin affects activation of TNF-α-induced NF-κB and myocardin/serum response factor (SRF) to convey hypertrophy signaling in cardiac myoblasts. In canine cardiac myoblasts, treatment with high insulin (10−8 to 10−7 m) for 0–24 h increased insulin receptor substrate (IRS)-1 phosphorylation at Ser-307, decreased protein levels of chaperone-associated ubiquitin (Ub) E3 ligase C terminus of heat shock protein 70-interacting protein (CHIP), increased SRF activity, as well as β-myosin heavy chain (MHC) and myocardin expressions. Here siRNAs to myocardin or NF-κB, as well as CHIP overexpression prevented (while siRNA-mediated CHIP disruption potentiated) high insulin-induced SR element (SRE) activation and β-MHC expression. Insulin markedly potentiated TNF-α-induced NF-κB activation. Compared with insulin alone, insulin+TNF-α increased SRF/SRE binding and β-MHC expression, which was reversed by the NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) and by NF-κB silencing. In the hearts of db/db diabetic mice, in which Akt phosphorylation was decreased, p38MAPK, Akt1, and IRS-1 phosphorylation at Ser-307 were increased, together with myocardin expression as well as SRE and NF-κB activities. In response to high insulin, cardiac myoblasts increase the expression or the promyogenic transcription factors myocardin/SRF in a CHIP-dependent manner. Insulin potentiates TNF-α in inducing NF-κB and SRF/SRE activities. In hyperinsulinemic states, myocardin may act as a nuclear effector of insulin, promoting cardiac hypertrophy.