Evaluation and Management of Reduced Dietary Diversity in Children with Pediatric Feeding Disorder.

Pediatric Feeding Disorder, a common problem in children, is commoner in children with various developmental disorders. Children with pediatric feeding disorder can have food selectivity and lack dietary diversity (DD). In this paper, an understanding of DD in these children is provided along with a dietary diversity index that can be helpful in measuring and understanding the risks posed by this lack of DD. An overview of a management strategy to address decreased DD is proposed. In these children, improving DD can improve growth, micronutrient status, long-term metabolic health, and potentially quality of life.

Using Toolkits to Improve Students' Skills in Advocacy.

BACKGROUND: Advocacy is widely recognized as a nursing responsibility. Speaking up, a form of advocacy, is known to benefit patient safety and quality of care yet research shows that nurses are hesitant to speak up and face multiple barriers when deciding to do so. METHOD: A toolkit that included web-based learning modules and simulation experience with a standardized patient was developed to enhance advocacy skills in baccalaureate nursing students. Student perceptions of the efficacy of this approach were used to revise and improve toolkit materials. RESULTS: There were 131 participants over four semesters. Students reported the toolkit helped them understand how to use advocacy skills (87%), allowed them to use critical thinking (97%), and practice advocacy (94%). CONCLUSION: Educational experiences like this promote development of students' advocacy skills in a safe environment and can be used to bridge the gap between expectation and practice. [J Nurs Educ. 2022;61(10):599-602.].

Estimating Vaccine-Preventable COVID-19 Deaths Under Counterfactual Vaccination Scenarios in the United States

ImportanceWith an abundant supply of COVID-19 vaccines becoming available in spring and summer 2021, the major barrier to high vaccination rates in the United States has been a lack of vaccine demand. This has contributed to a higher rate of deaths from SARS-CoV-2 infections amongst unvaccinated individuals as compared to vaccinated individuals. It is important to understand how low vaccination rates directly impact deaths resulting from SARS-CoV-2 infections in unvaccinated populations across the United States. ObjectiveTo estimate a lower bound on the number of vaccine-preventable deaths from SARS-CoV-2 infections under various scenarios of vaccine completion, for every state of the United States. Design, Setting, and ParticipantsThis counterfactual simulation study varies the rates of complete vaccination coverage under the scenarios of 100%, 90% and 85% coverage of the adult (18+) population of the United States. For each scenario, we use U.S. state-level demographic information in conjunction with county-level vaccination statistics to compute a lower bound on the number of vaccine-preventable deaths for each state. ExposuresCOVID-19 vaccines, SARS-CoV-2 infection Main Outcomes and MeasuresDeath from SARS-CoV-2 infection ResultsBetween January 1st, 2021 and April 30th, 2022, there were 641,305 deaths due to COVID-19 in the United States. Assuming each state continued peak vaccination capacity after initially achieving its peak vaccination rate, a vaccination rate of 100% would have led to 322,324 deaths nationally, that of 90% would have led to 415,878 deaths, and that of 85% would have led to 463,305 deaths. As a comparison, using the state with the highest peak vaccination rate (per million population each week) for all the states, a vaccination rate of 100% would have led to 302,344 deaths nationally, that of 90% would have led to 398,289 deaths, and that of 85% would have led to 446,449 deaths. Conclusions and RelevanceOnce COVID-19 vaccine supplies peaked across the United States, if there had been 100% COVID-19 vaccination coverage of the over 18+ population, a conservative estimate of 318,981 deaths could have been potentially avoided through vaccination. For a 90% vaccination coverage, we estimate at least 225,427 deaths averted through vaccination, and at least 178,000 lives saved through vaccination for an 85% vaccination coverage.

Evaluating and contextualizing the efficacy of portable HEPA filtration units in small exam rooms.

BACKGROUND: Ambulatory clinics attend to COVID-19 patients, often in spaces with less than ideal ventilation. Testing and treatments can often include aerosol-generating procedures. Portable high efficiency particulate air (HEPA) filtration units have been used to remove airborne contaminants in these areas. METHODS: A particle counter was used to evaluate the effectiveness of portable HEPA filtration units when a proxy airborne contaminant (powder) was actuated into the air. The Center for Disease Control and Prevention's (CDC) Airborne Contaminant Removal table served as a basis for initial particle readings at 6 minutes. RESULTS: Percent decrease was calculated post powder actuation at the 6-minute and 12-minute mark. There was a statistically significant decrease in smaller particles at the 6-minute and 12-minute mark when the HEPA filtration units were used. CONCLUSION: As an adjunct infection control intervention, portable HEPA filtration units can make outpatient exam rooms safer for patients and staff by decreasing cumulative airborne particles.

Impact of a contactless prescription pickup kiosk on prescription abandonment, patient experience, and pharmacist consultations.

OBJECTIVE: Investigate the impact of increased access to new and refilled prescriptions by means of an automated pickup kiosk (Asteres ScriptCenter) on prescription abandonment rates, patient experience, and pharmacist consultations. DESIGN: Nonrandomized, observational study using retrospective, deidentified data from the filling pharmacy, the kiosk, and a pharmacist-completed counseling documentation log over a 35-month study period. SETTING AND PARTICIPANTS: Hospital employees opting to use a kiosk located in the lobby with 24 hours a day, 7 days a week access for pickups and a telephone pharmacist consultation service compared with employees using the regular counter at the filling pharmacy. OUTCOME MEASURES: Return to stock (RTS) rate to assess prescription abandonment, time to prescription pickup, consultation duration, kiosk user assessment, and pharmacist assessment of counseling ability. RESULTS: Approximately 9% of employees (440) enrolled to use the kiosk, with 5062 kiosk pickups recorded for new prescriptions (29%), refill prescriptions (33%), and over-the-counters (38%). The mean kiosk RTS (4.3% ± 3.2) was lower than that at the regular counter (5.6% ± 0.8), P = 0.04, whereas the mean time to pickup was approximately 1 day greater at the kiosk than the regular counter (2.8 ± 0.4 vs. 1.8 ± 0.2, P < 0.001). The average kiosk consultation was approximately 1 minute shorter (2.0 ± 1.4) than that of the regular counter (3.4 ± 1.9, P < 0.001), and fewer patients using the kiosk (15.7%) had additional questions at the end of a consultation session than patients at the regular counter (38.8%, P < 0.001). Most of the kiosk users agreed that their prescription questions were answered and that kiosk convenience was an important reason for using the filling pharmacy. Almost all (>90%) pharmacists indicated that they were able to effectively counsel patients at the kiosk and the regular counter. CONCLUSION: The kiosk, used by self-selected health care workers located in a hospital workplace setting with 24 hours a day, 7 days a week access, was a convenient, contactless pickup extension of the filling pharmacy with a lower prescription abandonment rate and similar pickup and consultation characteristics as at the regular pharmacy counter.

Learning-induced ribosomal RNA is required for memory consolidation in mice-Evidence of differentially expressed rRNA variants in learning and memory.

The transition from short-term to long-term forms of synaptic plasticity requires protein synthesis and new gene expression. Most efforts to understand experience-induced changes in neuronal gene expression have focused on the transcription products of RNA polymerase II-primarily mRNAs and the proteins they encode. We recently showed that nucleolar integrity and activity-dependent ribosomal RNA (rRNA) synthesis are essential for the maintenance of hippocampal long-term potentiation (LTP). Consequently, the synaptic plasticity and memory hypothesis predicts that nucleolar integrity and activity dependent rRNA synthesis would be required for Long-term memory (LTM). We tested this prediction using the hippocampus-dependent, Active Place Avoidance (APA) spatial memory task and found that training induces de novo rRNA synthesis in mouse dorsal hippocampus. This learning-induced increase in nucleolar activity and rRNA synthesis persists at least 24 h after training. In addition, intra-hippocampal injection of the Pol I specific inhibitor, CX-5461 prior to training, revealed that de novo rRNA synthesis is required for 24 h memory, but not for learning. Using qPCR to assess activity-dependent changes in gene expression, we found that of seven known rRNA expression variants (v-rRNAs), only one, v-rRNA IV, is significantly upregulated right after training. These data indicate that learning induced v-rRNAs are crucial for LTM, and constitute the first evidence that differential rRNA gene expression plays a role in memory.

New ribosomes for new memories?

Widely thought to be a housekeeping process, the regulation and synthesis of rRNA emerges as a potentially central mechanism for the maintenance of synaptic plasticity and memory. We have recently shown that an essential component of late-phase synaptic plasticity is rRNA biosynthesis - the rate-limiting step in the production of new ribosomes. We hypothesize that a particular population of ribosomes is generated upon learning-associated neural activity to alter the rate of synthesis of plasticity factors at tagged synapses that will support the maintenance of synaptic plasticity and memory.

Nucleolar integrity is required for the maintenance of long-term synaptic plasticity.

Long-term memory (LTM) formation requires new protein synthesis and new gene expression. Based on our work in Aplysia, we hypothesized that the rRNA genes, stimulation-dependent targets of the enzyme Poly(ADP-ribose) polymerase-1 (PARP-1), are primary effectors of the activity-dependent changes in synaptic function that maintain synaptic plasticity and memory. Using electrophysiology, immunohistochemistry, pharmacology and molecular biology techniques, we show here, for the first time, that the maintenance of forskolin-induced late-phase long-term potentiation (L-LTP) in mouse hippocampal slices requires nucleolar integrity and the expression of new rRNAs. The activity-dependent upregulation of rRNA, as well as L-LTP expression, are poly(ADP-ribosyl)ation (PAR) dependent and accompanied by an increase in nuclear PARP-1 and Poly(ADP) ribose molecules (pADPr) after forskolin stimulation. The upregulation of PARP-1 and pADPr is regulated by Protein kinase A (PKA) and extracellular signal-regulated kinase (ERK)--two kinases strongly associated with long-term plasticity and learning and memory. Selective inhibition of RNA Polymerase I (Pol I), responsible for the synthesis of precursor rRNA, results in the segmentation of nucleoli, the exclusion of PARP-1 from functional nucleolar compartments and disrupted L-LTP maintenance. Taken as a whole, these results suggest that new rRNAs (28S, 18S, and 5.8S ribosomal components)--hence, new ribosomes and nucleoli integrity--are required for the maintenance of long-term synaptic plasticity. This provides a mechanistic link between stimulation-dependent gene expression and the new protein synthesis known to be required for memory consolidation.

What is the value and impact of the safety World Conference? Evaluators' reflections of safety 2012.

Using survey and documentary information collected as part of an evaluation of the 2012 conference, this paper reflects upon the value of the 2012 World Conference to attendees of the event. The results are discussed in the context of questions about what the purpose of conference is to the world injury prevention community and how they are organised. The evaluators challenge the community and future organisers to clarify what the purpose of these events are to better inform future evaluation activities.

Polyglutamine toxicity is controlled by prion composition and gene dosage in yeast.

Polyglutamine expansion causes diseases in humans and other mammals. One example is Huntington's disease. Fragments of human huntingtin protein having an expanded polyglutamine stretch form aggregates and cause cytotoxicity in yeast cells bearing endogenous QN-rich proteins in the aggregated (prion) form. Attachment of the proline(P)-rich region targets polyglutamines to the large perinuclear deposit (aggresome). Aggresome formation ameliorates polyglutamine cytotoxicity in cells containing only the prion form of Rnq1 protein. Here we show that expanded polyglutamines both with (poly-QP) or without (poly-Q) a P-rich stretch remain toxic in the presence of the prion form of translation termination (release) factor Sup35 (eRF3). A Sup35 derivative that lacks the QN-rich domain and is unable to be incorporated into aggregates counteracts cytotoxicity, suggesting that toxicity is due to Sup35 sequestration. Increase in the levels of another release factor, Sup45 (eRF1), due to either disomy by chromosome II containing the SUP45 gene or to introduction of the SUP45-bearing plasmid counteracts poly-Q or poly-QP toxicity in the presence of the Sup35 prion. Protein analysis confirms that polyglutamines alter aggregation patterns of Sup35 and promote aggregation of Sup45, while excess Sup45 counteracts these effects. Our data show that one and the same mode of polyglutamine aggregation could be cytoprotective or cytotoxic, depending on the composition of other aggregates in a eukaryotic cell, and demonstrate that other aggregates expand the range of proteins that are susceptible to sequestration by polyglutamines.

Interventions (other than pharmacological, psychosocial or psychological) for treating antenatal depression.

BACKGROUND: Although pregnancy was once thought of as a time of emotional well-being for many women, conferring 'protection' against psychiatric disorders, a recent meta-analysis of 21 studies suggests the mean prevalence rate for depression across the antenatal period is 10.7%, ranging from 7.4% in the first trimester to a high of 12.8% in the second trimester. Due to maternal treatment preferences and potential concerns about fetal and infant health outcomes, non-pharmacological treatment options are needed. OBJECTIVES: To assess the effects, on mothers and their families, of non-pharmacological/psychosocial/psychological interventions compared with usual antepartum care in the treatment of antenatal depression. SEARCH STRATEGY: We searched the Cochrane Pregnancy and Childbirth Group's Trials Register (August 2007), the Cochrane Collaboration Depression Anxiety and Neurosis Group's Trials Registers (CCDANCTR-Studies and CCDANCTR-References) (January 2007), the Cochrane Central Register of Controlled Trials (The Cochrane Library 2006, Issue 3), MEDLINE (1966 to January 2007), EMBASE (1980 to January 2007) and CINAHL (1982 to January 2007). We scanned secondary references and contacted experts in the field to identify other published or unpublished trials. SELECTION CRITERIA: All published, unpublished and ongoing randomised controlled trials of non-pharmacological/psychosocial/psychological interventions to treat antenatal depression. DATA COLLECTION AND ANALYSIS: All review authors independently participated in the evaluation of methodological quality and data extraction. . MAIN RESULTS: We included one US three-armed randomised controlled trial in this review, incorporating 61 outpatient antenatal women who met Diagnostic and Statistical Manual for Mental Disorders-IV criteria for major depression. Maternal massage, compared to non-specific acupuncture (control group), did not significantly decrease the number of women diagnosed with clinical depression immediately post-treatment (one trial, n = 38; risk ratio (RR) 0.80, 95% confidence interval (CI) 0.25 to 2.53) or at final assessment at 10 weeks' postpartum (one trial, n = 32; RR 1.93, 95% CI 0.37 to 10.01). Acupuncture specifically treating symptoms of depression, compared to non-specific acupuncture, did not significantly decrease the number of women diagnosed with clinical depression immediately post-treatment (one trial, n = 35; RR 0.48, 95% CI 0.11 to 2.13) or at final assessment at 10 weeks' postpartum (one trial, n = 32; RR 0.64, 95% CI 0.06 to 6.39). AUTHORS' CONCLUSIONS: The evidence is inconclusive to allow us to make any recommendations for massage therapy or depression-specific acupuncture for the treatment of antenatal depression. The included trial was too small with a non-generalisable sample, to make any recommendations.

Effects of ubiquitin system alterations on the formation and loss of a yeast prion.

The yeast prion [PSI+] is a self-propagating amyloidogenic isoform of the translation termination factor Sup35. Overproduction of the chaperone protein Hsp104 results in loss of [PSI+]. Here we demonstrate that this effect is decreased by deletion of either the gene coding for one of the major yeast ubiquitin-conjugating enzymes, Ubc4, or the gene coding for the ubiquitin-recycling enzyme, Ubp6. The effect of ubc4Delta on [PSI+] loss was increased by depletion of the Hsp70 chaperone Ssb but was not influenced by depletion of Ubp6. This indicates that Ubc4 affects [PSI+] loss via a pathway that is the same as the one affected by Ubp6 but not by Ssb. In the presence of Rnq1 protein, ubc4Delta also facilitates spontaneous de novo formation of [PSI+]. This stimulation is independent of [PIN+], the prion isoform of Rnq1. Numerous attempts failed to detect ubiquitinated Sup35 in the yeast extracts. While ubc4Delta and other alterations of ubiquitin system used in this work cause slight induction of some Hsps, these changes are insufficient to explain their effect on [PSI+]. However, ubc4Delta increases the proportion of the Hsp70 chaperone Ssa bound to Sup35, suggesting that misfolded Sup35 is either more abundant or more accessible to the chaperones in the absence of Ubc4. The proportion of [PSI+] cells containing large aggregated Sup35 structures is also increased by ubc4Delta. We propose that UPS alterations induce an adaptive response, resulting in accumulation of the large "aggresome"-like aggregates that promote de novo prion generation and prion recovery from the chaperone treatment.

Developing a cultural competence assessment tool for people in recovery from racial, ethnic and cultural backgrounds: the journey, challenges and lessons learned.

In 1997, Maryland implemented a new managed care mental health system. Consumer satisfaction, evaluation and cultural competency were considered high priorities for the new system. While standardized tools for measuring consumer satisfaction were readily available, no validated, reliable and standardized tool existed to measure the perception of people from minority groups receiving mental health services. The MHA*/MHP* Cultural Competency Advisory Group (CCAG) accepted the challenge of developing a consumer assessment tool for cultural competency. The CCAG, composed of people in recovery, clinicians and administrators used their collective knowledge and experiences to develop a 52-item tool that met standards for validity and reliability. Consultation from a researcher helped to further develop the tool into one possessing tremendous potential for statewide implementation within Maryland's Public Mental Health System. Recognizing the limitations of the study and the need for further research, this instrument is a work in progress. Strategies to improve the instrument are currently underway with the Mental Hygiene Administration's Systems Evaluation Center of the University of Maryland and several national researchers.

Hsp70 chaperones as modulators of prion life cycle: novel effects of Ssa and Ssb on the Saccharomyces cerevisiae prion [PSI+].

[PSI(+)] is a prion isoform of the yeast release factor Sup35. In some assays, the cytosolic chaperones Ssa1 and Ssb1/2 of the Hsp70 family were previously shown to exhibit "pro-[PSI(+)]" and "anti-[PSI(+)]" effects, respectively. Here, it is demonstrated for the first time that excess Ssa1 increases de novo formation of [PSI(+)] and that pro-[PSI(+)] effects of Ssa1 are shared by all other Ssa proteins. Experiments with chimeric constructs show that the peptide-binding domain is a major determinant of differences in the effects of Ssa and Ssb proteins on [PSI(+)]. Surprisingly, overproduction of either chaperone increases loss of [PSI(+)] when Sup35 is simultaneously overproduced. Excess Ssa increases both the average size of prion polymers and the proportion of monomeric Sup35 protein. Both in vivo and in vitro experiments uncover direct physical interactions between Sup35 and Hsp70 proteins. The proposed model postulates that Ssa stimulates prion formation and polymer growth by stabilizing misfolded proteins, which serve as substrates for prion conversion. In the case of very large prion aggregates, further increase in size may lead to the loss of prion activity. In contrast, Ssb either stimulates refolding into nonprion conformation or targets misfolded proteins for degradation, in this way counteracting prion formation and propagation.

Pleiotropic effects of Ubp6 loss on drug sensitivities and yeast prion are due to depletion of the free ubiquitin pool.

Mutation of the mouse Usp14 gene, encoding the homolog of yeast deubiquitinating enzyme Ubp6, causes ataxia. Here we show that deletion of the UBP6 gene in Saccharomyces cerevisiae causes sensitivity to a broad range of toxic compounds and antagonizes phenotypic expression and de novo induction of the yeast prion [PSI+], a functionally defective self-perpetuating isoform of the translation termination factor Sup35. Conversely, overexpression of ubiquitin (Ub) increases phenotypic expression and induction of [PSI+] in the wild type cells and suppresses all tested ubp6Delta defects, indicating that they are primarily due to depletion of cellular Ub levels. Several lines of evidence suggest that Ubp6 functions on the proteasome. First, Ub levels in the ubp6Delta cells can be partly restored by proteasome inhibitors, suggesting that deletion of Ubp6 decreases Ub levels by increasing proteasome-dependent degradation of Ub. Second, fluorescence microscopy analysis shows that Ubp6-GFP fusion protein is localized to the nucleus of yeast cell, as are most proteasomes. Third, the N-terminal Ub-like domain, although it is not required for nuclear localization of Ubp6, targets Ubp6 to the proteasome and cannot be functionally replaced by Ub. The human ortholog of Ubp6, USP14, probably plays a similar role in higher eukaryotes, since it fully compensates for ubp6Delta defects and binds to the yeast proteasome. These data link the Ub system to prion expression and propagation and have broad implications for other neuronal inclusion body diseases.