School Wellness Committees Are Associated With Lower Body Mass Index Z‐Scores and Improved Dietary Intakes in US Children: The Healthy Communities Study

BACKGROUND

Our objective was to examine the association between school wellness committees and implementation of nutrition wellness policies and children's weight status and obesity‐related dietary outcomes.

METHODS

A cross‐sectional study was conducted of 4790 children aged 4‐15 years recruited from 130 communities in the Healthy Communities Study. Multilevel statistical models assessed associations between school wellness policies and anthropometric (body mass index z‐score [BMIz]) and nutrition measures, adjusting for child and community‐level covariates.

RESULTS

Children had lower BMI z‐scores (?0.11, 95% confidence interval [CI]: ?0.19, ?0.03) and ate breakfast more frequently (0.14 days/week, 95% CI: 0.02‐0.25) if attending a school with a wellness committee that met once or more in the past year compared to attending a school with a wellness committee that did not meet/did not exist. Children had lower added sugar (p < .0001), lower energy‐dense foods (p = .0004), lower sugar intake from sugar‐sweetened beverages (p = .0002), and lower dairy consumption (p = .001) if attending a school with similar or stronger implementation of the nutrition components of the school wellness policies compared to other schools in the district.

CONCLUSIONS

A more active wellness committee was associated with lower BMI z‐scores in US schoolchildren. Active school engagement in wellness policy implementation appears to play a positive role in efforts to reduce childhood obesity.

     

Altered tension cost in (TG(mREN-2)27) rats overexpressing the mouse renin gene

The present study aimed to characterize cardiac hypertrophy induced by activation of the renin–angiotensin system in terms of functional alterations on the level of the contractile proteins, employing transgenic rats harboring the mouse renin gene (TGR(mREN2)27). Ca²⁺-dependent tension and myosin ATPase activity were measured in skinned fiber preparations obtained from TGR(mREN2)27 and from age-matched Sprague–Dawley rats (SPDR). Western blots for troponin I (TnI) and troponin T (TnT) were performed and the phosphorylation status of TnI were evaluated in myocardial preparations. TnT and myosin heavy chain (MHC) isoforms were analyzed by RT-PCR. The pCa/tension relationship was shifted to the right in TGR(mREN2)27 compared to SPDR as indicated by increased Ca²⁺-concentrations required for half maximal activation of tension (SPDR 5.80, 95% confidence limits 5.77–5.82 vs. TGR(mREN2)27 5.69, 95% confidence limits 5.67–5.72, pCa units), while maximal developed tension was unaltered. Even more pronounced was the shift in the relationship between pCa and myosin–ATPase (SPDR 6.01, 95% confidence limits 5.99–6.03 vs. TGR(mREN2)27 5.77, 95% confidence limits 5.73–5.79, pCa units). The maximal myosin–ATPase activity was reduced in TGR(mREN2)27 compared to SPDR, respectively (211.0 ± 28.77 μmol ADP/s vs. 271.6 ± 43.66 μmol ADP/s, P < 0.05). Tension cost (ATPase activity/tension) was significantly reduced in TGR(mREN2)27. The β-MHC expression was significantly increased in TGR(mREN2)27. There was no isoform shift for TnT (protein and mRNA), as well as TnI, and no alteration of the phosphorylation of TnI in TGR(mREN2)27 compared to SPRD. The present study demonstrates that cardiac hypertrophy, induced by an activation of the renin–angiotensin system, leads to adapting alterations on the level of the contractile filaments, which reduce tension cost.     

Interference of contaminated sediment extracts and environmental pollutants with retinoid signaling

Retinoids are known to regulate important processes such as differentiation, development, and embryogenesis. Some effects, such as malformations in frogs or changes in metabolism of birds, could be related to disruption of the retinoid signaling pathway by exposure to organic contaminants. A new reporter gene assay has been established for evaluation of the modulation of retinoid signaling by individual chemicals or environmental samples. The bioassay is based on the pluripotent embryonic carcinoma cell line P19 stably transfected with the firefly luciferase gene under the control of a retinoic acid-responsive element (clone P19/ A15). The cell line was used to characterize the effects of individual chemicals and sediments extracts on retinoid signaling pathways. The extracts of sediments from the River Kymi, Finland, which contained polychlorinated dioxins and furans and polycyclic aromatic hydrocarbons (PAHs), significantly increased the potency of all-trans retinoic acid (ATRA), while no effect was observed with the extract of the sediment from reference locality. Considerable part of the effect was caused by the labile fraction of the sediment extracts. Also, several individual PAHs potentiated the effect of ATRA; on the other hand, 2,3,7,8-tetrachlorodibenzo-p-dioxin and several phthalates showed slightly inhibiting effect. These results suggest that PAHs could be able to modulate the retinoid signaling pathway and that they could be responsible for a part of the proretinoid activity observed in the sediment extracts. However, the effects of PAHs on the retinoic acid signaling pathways do not seem to be mediated directly by crosstalk with aryl hydrocarbon receptor.     

Effects of plasma nitric oxide levels on platelet activation in single donor apheresis and random donor concentrates.

P-selectin is an useful marker to determine platelet activation and nitric oxide inhibits platelet activation, secretion, adhesion and aggregation. The aim of this study was to investigate the relationship between nitric oxide and P-selectin values in both single donor apheresis and random donor platelet concentrates. According to the results of this study, we found that the best platelet concentrate is freshly prepared single donor apheresis concentrate and it is important to prevent activation at the beginning of the donation. Nitric oxide, which is synthesized from platelets during the storage period, is not sufficient to prevent platelet activation.     

The Unenlarged Lymph Nodes of HIV-1–infected, Asymptomatic Patients with High CD4 T Cell Counts Are Sites for Virus Replication and CD4 T Cell Proliferation. The Impact of Highly Active Antiretroviral Therapy

The efficacy of triple drug therapy for HIV-1 infection encourages its early use to prevent damage to the immune system. We monitored the effects of such therapy on 12 patients with 14–75-mo histories of minimal disease, i.e., CD4⁺ counts constantly >500/μl and little or no lymph node enlargement. In this way, we could first determine the extent of viral replication and immunoarchitectural changes in unenlarged nodes early in disease, and second follow the response to triple therapy in plasma and lymphoid tissue in tandem. As is known for lymph nodes with more advanced disease, the germinal centers showed productively infected T cells, i.e., CD4⁺CD1a⁻CD68⁻ cells labeling intensely for HIV-1 RNA after in situ hybridization. The unenlarged nodes also showed extensive HIV-1 RNA retention on a well-preserved, follicular dendritic cell (FDC) network, and the follicles were abnormal. There were numerous CD8⁺ cells, many expressing TIA-1 granule antigen. Also, in contrast to normal follicles, CD4⁺ T cell proliferation was active, with marked increases in the number of cycling, Ki-67⁺CD4⁺CD45R0⁺ cells. After 28 d and 3 mo of therapy, productively infected T cells decreased dramatically and often were not apparent. The labeling of the FDC network for viral RNA also decreased, but not for gag protein. We conclude that HIV-1 replicates and accumulates in lymphoid organs before damage of the immune system, that at this stage of disease de novo production of T cells occurs in the lymphoid tissue, and that the infection is sensitive to triple drug therapy in both plasma and lymph nodes.     

Interprofessional Communication Patterns During Patient Discharges: A Social Network Analysis

BACKGROUND

Optimal care delivery requires timely, efficient, and accurate communication among numerous providers and their patients, especially during hospital discharge. Little is known about communication patterns during this process.

OBJECTIVE

Our aim was to assess the frequency and patterns of communication between patients and providers during patient discharges from a hospital-based medicine unit.

DESIGN AND APPROACH

On the day of the patient’s discharge, the patient and all healthcare providers involved in the discharge were interviewed using structured questions related to information exchange during the discharge process. Each interview identified the frequency and method of communication between participants, including synchronous (e.g., face-to-face) and asynchronous (e.g., through electronic medical record) routes. Communication patterns were visually diagramed using social network analysis.

PARTICIPANTS

Forty-six patients were screened for inclusion in the network analysis. Of those, seven patients who were fully oriented and able to complete an interview and all providers who participated in their care during the discharge were selected for inclusion in the analysis. In all, 72 healthcare professionals contributing to the discharge process were interviewed, including physicians, nurses, therapists, pharmacists, care coordinators, social workers, and nutritionists.

KEY RESULTS

Patients’ mean age was 63, length-of-stay was 7.8 days, and most (86 %) were discharged to home. On average, 11 roles were involved with each discharge. The majority of communication was synchronous (562 events vs. 469 asynchronous events, p = 0.004). Most communication events occurred between the primary nurse and patient and the care coordinator and primary nurse (mean 3.9 and 2.3 events/discharge, respectively). Participants identified intern physicians as most important in the discharge process, followed by primary nurses and care coordinators.

CONCLUSIONS

In patients being discharged from the medicine service, communication was more frequently synchronous, and occurred between intern physicians, primary nurses, and patients. Potential improvements in coordinating patients’ discharges are possible by reorganizing systems to optimize efficient communication.

Electronic supplementary material

The online version of this article (doi:10.1007/s11606-015-3415-2) contains supplementary material, which is available to authorized users.     

Differences in gastroprotective processes in 6- to 8- and 14- to 16-week-old rats

The gastroprotective effect of opioid peptides, prostaglandin E₂ and capsaicin against acidified ethanol-induced gastric mucosal damage in young mature rats of different (6–8 and 14–16 weeks) ages has been investigated. It was found that gastric mucosal damage was more severe in 14–16 weeks old rats. The gastroprotective effect of opioid peptides - [D-Ala², D-Leu⁵]-enkephalin (DADLE), deltorphin II, [D-Ala², Phe⁴, Gly⁵ -ol]-enkephalin (DAGO) and -endorphin - given either intracerebroventricularly (0.6, 3.3., 0.2, and 0.01 nmol/rat, respectively) or subcutaneously (825 and 960 nmol/kg, respectively) was highly reduced in 14–16 weeks old rats. The mucosal protective action of orally administered capsaicin (1600–3200 nmol/kg) and PGE₂ (280–560 nmol/kg) was also diminished in 14–16 weeks old animals. Both ACTH and corticosterone plasma levels were significantly higher in 14–16 weeks old rats. These results suggest that the gastric mucosal susceptibility to ethanol and the gastroprotective effect of opioid peptides, capsaicin and PGE₂ are age-related.