Dietary studies of children from a biracial population: intakes of vitamins in 10- and 13-year-olds.

Impact of vitamin supplements upon dietary intakes of eight vitamins was examined in 10- and 13-year-old children randomly selected from a biracial community, Bogalusa, LA. More younger children reported taking supplements daily (17%) than did adolescents (12%). Over 90% of the children surveyed had dietary intakes of vitamin E and niacin that met or exceeded the RDA. One-half to two-thirds of children using supplements had adequate intakes of ascorbic acid from diet alone. Children who most needed ascorbic acid supplements were the least likely to take them. One-quarter to one-half of the children did not consume the RDA levels of vitamin A, thiamine, and riboflavin. Adolescents had less adequate vitamin A intakes than younger children. In all surveys, a higher proportion of girls than boys had intakes that did not meet the RDA for vitamins B6 and B12. Vitamin intakes of Bogalusa children and adolescents were comparable to other U.S. surveys. Inclusion of vitamin E and niacin in supplements may be unnecessary.     

Enhancing social networks: a qualitative study of health and social care practice in UK mental health services

People with severe mental health problems such as psychosis have access to less social capital, defined as resources within social networks, than members of the general population. However, a lack of theoretically and empirically informed models hampers the development of social interventions which seek to enhance an individual's social networks. This paper reports the findings of a qualitative study, which used ethnographic field methods in six sites in England to investigate how workers helped people recovering from psychosis to enhance their social networks. This study drew upon practice wisdom and lived experience to provide data for intervention modelling. Data were collected from 73 practitioners and 51 people who used their services in two phases. Data were selected and coded using a grounded theory approach to depict the key themes that appeared to underpin the generation of social capital within networks. Findings are presented in four over‐arching themes – worker skills, attitudes and roles; connecting people processes; role of the agency; and barriers to network development. The sub‐themes which were identified included worker attitudes; person‐centred approach; equality of worker–individual relationship; goal setting; creating new networks and relationships; engagement through activities; practical support; existing relationships; the individual taking responsibility; identifying and overcoming barriers; and moving on. Themes were consistent with recovery models used within mental health services and will provide the basis for the development of an intervention model to enhance individuals’ access to social capital within networks.     

The Impact of Work‐Limiting Disability on Labor Force Participation

According to the justification hypothesis, non‐employed individuals may over‐report their level of work limitation, leading to biased census/survey estimates of the prevalence of severe disabilities and the associated labor force participation rate. For researchers studying policies which impact the disabled or elderly (e.g., Supplemental Security Income, Disability Insurance, and Early Retirement), this could lead to significant bias in key parameters of interest. Using the American Community Survey, we examine the potential for both inflated and deflated reported disability status and generate a general index of disability, which can be used to reduce the bias of these self‐reports in other studies. We find that at least 4.8 million individuals have left the labor force because of a work‐limiting disability, at least four times greater than the impact implied by our replication of previous models. Copyright © 2013 John Wiley & Sons, Ltd.     

Substrate for endothelial prostacyclin production in the presence of platelets exposed to collagen is derived from the platelets rather than the endothelium

Interactions between vascular endothelial cells and blood platelets have been investigated using a model microcirculation consisting of microcarrier beads colonized with human umbilical vein endothelial cells (HUVECs) and perfused with washed platelet suspensions. To simulate the effects of endothelial desquamation and exposure of subendothelium, fibrillar collagen in suspension was coinjected with the platelets. In this model, neither the passage of platelets alone nor collagen alone stimulated prostacyclin (PGI2) production by the HUVECs. Platelets activated by coinjection with collagen released thromboxane A2 (TXA2), and this was associated with the simultaneous production of PGI2 by the HUVECs. By means of double-isotope experiments with [3H]arachidonic acid (AA) incorporated into platelets and [14C]-AA into HUVECs, it was shown that all the PGI2 generated was derived from platelet AA and/or endoperoxides. This interpretation was strengthened by the finding that PGI2 production was not prevented by treatment of HUVECs with indomethacin followed by perfusion with collagen-stimulated platelets. AA metabolites in double-isotope label experiments were further characterized by reverse-phase chromatography, and it was shown that both cyclooxygenase and lipoxygenase products of the HUVECs were derived from platelet membrane lipid. Thrombin regularly produced transient PGI2 release, but showed rapid tachyphylaxis. Platelet-derived compounds including ADP, ATP, and platelet-activating factor (PAF) did not produce PGI2 release by HUVECs in this system. Thus, the transfer of AA and metabolites from collagen- stimulated platelets is likely to be the mechanism for PGI2 production in the context of minor degrees of endothelial desquamation.     

Serum lipoprotein profile in children from a biracial community: the Bogalusa Heart Study.

Serum lipoprotein profiles in 3182 children, ages 5-14 years, were studied in a biracial community as part of the Bogalusa Heart Study to describe the early natural history of atherosclerosis. White and black children showed similar mean levels of beta-lipoproteins. Pre-beta-lipoprotein levels, however, were significantly higher in white shildren, while significantly higher levels of alpha-lipoprotein were found in black children. Girls had generally higher levels of beta- and pre-beta-lipoprotein and lower levels of alpha-lipoprotein than boys, although the differences were not significant at each age group. With age there was little change in alpha-lipoprotein levels, a significant increase in pre-beta-lipoprotein levels and a slight but significant decrease between 11 and 14 years in beta-lipoprotein levels. The correlation of alpha-lipoprotein was negative with beta-lipoprotein and, to a greater extent, with pre-beta-lipoprotein. The above inverse relationships were significantly greater in white children than in black children, suggesting differences in lipoprotein profiles in the two groups. Lipoprotein values from a total community study are now available for comparison with the currently recommended upper normal limits for lipoproteins. Since only a very small percentage of children could be considered as hyperlipoproteinemic by those specific levels in this community, we suggest that distributions and percentiles be used to evaluate children for hyperlipoproteinemia.     

Outcomes for children with acute myocarditis

The optimum treatment for myocarditis in children is unknown. We present outcomes for this disease as seen in a large series of children. Thus, we identified all children seen with myocarditis at Children's Hospital of Pittsburgh since 1985, including only those with biopsy-proven myocarditis, or cardiac dysfunction and proof of concomitant cardiotropic viral infection. Outcomes were defined as complete recovery, incomplete recovery, and death or transplantation. We identified 41 patients, 37 proven by histology, and 4 patients who were too unstable for biopsy but had proof of viral infection. Of the group, 27 (66%) made a complete recovery, 4 (10%) had incomplete recovery, and 10 (24%) either died (5) or underwent transplantation (5). The median time to death or transplantation was 8.4 months, with a range from 1 day to 49 months. Steroids had been administered to 16 patients, of whom 10 made a complete recovery, 2 an incomplete recovery, 2 died, and 2 were transplanted. Intravenous immune globulin was given in isolation to one patient, who made a complete recovery, and to 18 in combination with steroids, of whom 12 made a complete recovery, 2 an incomplete recovery, 2 died, and 2 were transplanted. The remaining 6 patients received neither steroids nor intravenous immune globulin, and of these, 4 made a complete recovery, 1 was transplanted, and 1 died. Freedom from death or transplantation was 81% at 1 year, and 74% at 5 years, with no difference between the modes of treatments. The median time to recovery of function was also comparable between the groups. Thus, in our patients, treatment with intravenous immune globulin appeared to confer no advantage to steroid therapy alone. These data emphasise the need for randomised trials to assess the efficacy of current treatments, as well as that of new therapies.     

A comparison of salbutamol given by pressure-packed aerosol or nebulization via IPPB in acute asthma.

Salbutamol was given by pressure-packed aerosol or nebulizer via IPPB to patients with acute asthma to compare the effectiveness of these methods of inhalation. The results show that both methods produce significant bronchodilatation even in patients admitted with moderately severe asthma (FEV1 about 38% predicted) but a slightly greater improvement may be achieved by IPPB nebulization. Our findings indicate that supervised inhalation of a pressure-packed aerosol of salbutamol may be useful for the initial treatment of asthmatic attacks but confirm the marginal advantage of IPPB nebulization, which should be reserved for patients unable to inhale from a pressure-packed aerosol or failing to respond to its treatment.     

Age-determined expression of priming protease TMPRSS2 and localization of SARS-CoV-2 in lung epithelium

The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) novel coronavirus 2019 (COVID-19) global pandemic has led to millions of cases and hundreds of thousands of deaths. While older adults appear at high risk for severe disease, hospitalizations and deaths due to SARS-CoV-2 among children have been relatively rare. Integrating single-cell RNA sequencing (scRNA-seq) of developing mouse lung with temporally resolved immunofluorescence in mouse and human lung tissue, we found that expression of SARS-CoV-2 Spike protein primer TMPRSS2 was highest in ciliated cells and type I alveolar epithelial cells (AT1), and TMPRSS2 expression increased with aging in mice and humans. Analysis of autopsy tissue from fatal COVID-19 cases detected SARS-CoV-2 RNA most frequently in ciliated and secretory cells in airway epithelium and AT1 cells in peripheral lung. SARS-CoV-2 RNA was highly colocalized in cells expressing TMPRSS2. Together, these data demonstrate the cellular spectrum infected by SARS-CoV-2 in lung epithelium and suggest that developmental regulation of TMPRSS2 may underlie the relative protection of infants and children from severe respiratory illness.     

Parental origin of mutation and the risk of breast cancer in a prospective study of women with a BRCA1 or BRCA2 mutation

The objective is to estimate the risk of breast cancer in women who carry a deleterious BRCA1 or BRCA2 mutation, according to parental origin of mutation. We conducted a cohort study of women with a BRCA1 mutation (n = 1523) or BRCA2 mutation (n = 369) who had not been diagnosed with breast or ovarian cancer. For each woman, the pedigree was reviewed and the origin of the mutation was assigned as probable paternal or maternal. The hazard ratio (HR) for developing breast cancer in the follow‐up period was estimated for women with a paternal mutation compared to a maternal mutation. The risk of breast cancer was modestly higher in women with a paternal BRCA1 mutation compared to women with a maternal BRCA1 mutation (HR = 1.46; 95% CI = 0.99–2.16) but the difference was not significant (p = 0.06). The parental mutation origin did not affect the risk in women with a BRCA2 mutation. Our results are consistent with the hypothesis that there is an increased risk of breast cancer among women with a paternally inherited BRCA1 mutation compared to a maternally inherited mutation. However, the data are not sufficiently compelling to justify different screening recommendations for the two subgroups.