Screening for and Diagnosing Malnutrition in Hospitalized Pediatric Patients

Background: Malnutrition is often underdiagnosed, and consequently undertreated, in hospitalized patients. A nationwide study is being conducted to validate indicators (the Malnutrition Clinical Characteristics [MCC]) to diagnose malnutrition in hospitalized patients. Methods: For the full study, sixty pediatric hospitals will collect patient medical history, patient STRONGKids malnutrition screening score, and nutrition intervention data. Six hundred pediatric patients will be randomly selected from the cohort to be assessed for the MCC and the Nutrition Focused Physical Exam (NFPE). Medical outcomes will be collected for all patients for a three-month period thereafter. Baseline data from a subset of sites that have started data collection were descriptively analyzed using Stata 15. Results: As of March 2020, 113 pediatric patients are enrolled in the study, with 50 children ages 1-24 months and 63 children and adolescents ages 2-17. Based on the STRONGkids screener, 73% (n = 82) of participants were “at risk” for malnutrition. A higher proportion of participants in the older age group screened at risk (n=54; 86%) compared to the younger group (n=28; 56%). Fifty-seven of the 113 participants were included in the MCC subgroup, of whom 35 (61%) screened at-risk for malnutrition. Based on the MCC criteria, 49% (n = 28) were diagnosed with malnutrition. Inadequate nutrient intake was the MCC indicator most often used to support a malnutrition diagnosis in younger participants, while weight loss was the most commonly used indicator for older participants. Across both age groups, muscle wasting and subcutaneous fat loss were the most commonly reported NFPE indicators that further supported a malnutrition diagnosis. Conclusion: Screening-based risk for malnutrition and malnutrition indicators differ for infants and young children compared to older children and teens. Differences in risk factors for malnutrition by age group and the validity of the MCC will be assessed as more data are collected

Devotions for Advent 2023 Return & Rebuild The Temple of God An Advent & Christmastide Devotional

Greetings in the name of Christ! Across two seminaries, across several states, and across this Advent and Christmastide, we have gathered devotions from several students- both at CTSFW and CSL- to guide us in our consideration of this season. As new theologians and workers in the Church, we have a chance to encourage our brothers and sisters and stir each other up to look to Christ. So who is this Christ? He is the culmination of the entire Scriptures, and so we find Him everywhere. The books of Ezra and Haggai are center stage in the Advent portion: God provides a way to return, to contribute to the presence of God among His people by building His Temple. Yes, Advent is a penitential season, a season of recognizing our vocations and how we have fallen short- but also how Christ comes among us nevertheless. We all have a part to play in rebuilding the body of Christ, the true Temple of God. Let not fear of our persecutors rule over us, because God will shame them and vindicate those who wait for Him! In the joy of Christmastide, enjoy the season with a smattering of texts and devotions (as well as 3 sermons!) on the fulfillment of God’s Temple, the incarnate God! What Zerubabbel sought to accomplish, Christ has fulfilled, and He will not let us go without a reminder of our duties to the Church. His body is worthy of every gift we can bring! The Church is now God’s Temple, and even our individual bodies. How great a stewardship that we have, to build up the Body of the crucified, risen, and ascended Lord! Indeed, God’s manifold word, both Law and Gospel, have much to say to us this season. Thank you to all who contributed your wisdom and meditations for the communities’ use- and may God bless your reading and prayer.https://scholar.csl.edu/osp/1024/thumbnail.jp

Glutathione Restores the Mechanism of Synaptic Plasticity in Aged Mice to That of the Adult

Glutathione (GSH), the major endogenous antioxidant produced by cells, can modulate the activity of N-methyl-D-aspartate receptors (NMDARs) through its reducing functions. During aging, an increase in oxidative stress leads to decreased levels of GSH in the brain. Concurrently, aging is characterized by calcium dysregulation, thought to underlie impairments in hippocampal NMDAR-dependent long-term potentiation (LTP), a form of synaptic plasticity thought to represent a cellular model for memory

Long-Term Continental Changes in Wing Length, but Not Bill Length, of a Long-Distance Migratory Shorebird

We compiled a >50‐year record of morphometrics for semipalmated sandpipers (Calidris pusilla), a shorebird species with a Nearctic breeding distribution and intercontinental migration to South America. Our data included >57,000 individuals captured 1972–2015 at five breeding locations and three major stopover sites, plus 139 museum specimens collected in earlier decades. Wing length increased by ca. 1.5 mm (>1%) prior to 1980, followed by a decrease of 3.85 mm (nearly 4%) over the subsequent 35 years. This can account for previously reported changes in metrics at a migratory stopover site from 1985 to 2006. Wing length decreased at a rate of 1,098 darwins, or 0.176 haldanes, within the ranges of other field studies of phenotypic change. Bill length, in contrast, showed no consistent change over the full period of our study. Decreased body size as a universal response of animal populations to climate warming, and several other potential mechanisms, are unable to account for the increasing and decreasing wing length pattern observed. We propose that the post‐WWII near‐extirpation of falcon populations and their post‐1973 recovery driven by the widespread use and subsequent limitation on DDT in North America selected initially for greater flight efficiency and latterly for greater agility. This predation danger hypothesis accounts for many features of the morphometric data and deserves further investigation in this and other species

HER2-enriched subtype and novel molecular subgroups drive aromatase inhibitor resistance and an increased risk of relapse in early ER+/HER2+ breast cancer

BACKGROUND: Oestrogen receptor positive/ human epidermal growth factor receptor positive (ER+/HER2+) breast cancers (BCs) are less responsive to endocrine therapy than ER+/HER2- tumours. Mechanisms underpinning the differential behaviour of ER+HER2+ tumours are poorly characterised. Our aim was to identify biomarkers of response to 2 weeks’ presurgical AI treatment in ER+/HER2+ BCs. METHODS: All available ER+/HER2+ BC baseline tumours (n=342) in the POETIC trial were gene expression profiled using BC360™ (NanoString) covering intrinsic subtypes and 46 key biological signatures. Early response to AI was assessed by changes in Ki67 expression and residual Ki67 at 2 weeks (Ki672wk). Time-To-Recurrence (TTR) was estimated using Kaplan-Meier methods and Cox models adjusted for standard clinicopathological variables. New molecular subgroups (MS) were identified using consensus clustering. FINDINGS: HER2-enriched (HER2-E) subtype BCs (44.7% of the total) showed poorer Ki67 response and higher Ki672wk (p<0.0001) than non-HER2-E BCs. High expression of ERBB2 expression, homologous recombination deficiency (HRD) and TP53 mutational score were associated with poor response and immune-related signatures with High Ki672wk. Five new MS that were associated with differential response to AI were identified. HER2-E had significantly poorer TTR compared to Luminal BCs (HR 2.55, 95% CI 1.14–5.69; p=0.0222). The new MS were independent predictors of TTR, adding significant value beyond intrinsic subtypes. INTERPRETATION: Our results show HER2-E as a standardised biomarker associated with poor response to AI and worse outcome in ER+/HER2+. HRD, TP53 mutational score and immune-tumour tolerance are predictive biomarkers for poor response to AI. Lastly, novel MS identify additional non-HER2-E tumours not responding to AI with an increased risk of relapse

Abstracts from the NIHR INVOLVE Conference 2017

n/

Carboplatin in BRCA1/2-mutated and triple-negative breast cancer BRCAness subgroups: the TNT Trial

Germline mutations in BRCA1/2 predispose individuals to breast cancer (termed germline-mutated BRCA1/2 breast cancer, gBRCA-BC) by impairing homologous recombination (HR) and causing genomic instability. HR also repairs DNA lesions caused by platinum agents and PARP inhibitors. Triple-negative breast cancers (TNBCs) harbor subpopulations with BRCA1/2 mutations, hypothesized to be especially platinum-sensitive. Cancers in putative ‘BRCAness’ subgroups—tumors with BRCA1 methylation; low levels of BRCA1 mRNA (BRCA1 mRNA-low); or mutational signatures for HR deficiency and those with basal phenotypes—may also be sensitive to platinum. We assessed the efficacy of carboplatin and another mechanistically distinct therapy, docetaxel, in a phase 3 trial in subjects with unselected advanced TNBC. A prespecified protocol enabled biomarker–treatment interaction analyses in gBRCA-BC and BRCAness subgroups. The primary endpoint was objective response rate (ORR). In the unselected population (376 subjects; 188 carboplatin, 188 docetaxel), carboplatin was not more active than docetaxel (ORR, 31.4% versus 34.0%, respectively; P = 0.66). In contrast, in subjects with gBRCA-BC, carboplatin had double the ORR of docetaxel (68% versus 33%, respectively; biomarker, treatment interaction P = 0.01). Such benefit was not observed for subjects with BRCA1 methylation, BRCA1 mRNA-low tumors or a high score in a Myriad HRD assay. Significant interaction between treatment and the basal-like subtype was driven by high docetaxel response in the nonbasal subgroup. We conclude that patients with advanced TNBC benefit from characterization of BRCA1/2 mutations, but not BRCA1 methylation or Myriad HRD analyses, to inform choices on platinum-based chemotherapy. Additionally, gene expression analysis of basal-like cancers may also influence treatment selection

Prolonged rote learning produces delayed memory facilitation and metabolic changes in the hippocampus of the ageing human brain

Background: Repeated rehearsal is one method by which verbal material may be transferred from short- to long-term memory. We hypothesised that extended engagement of memory structures through prolonged rehearsal would result in enhanced efficacy of recall and also of brain structures implicated in new learning. Twenty-four normal participants aged 55-70 (mean = 60.1) engaged in six weeks of rote learning, during which they learned 500 words per week every week (prose, poetry etc.). An extensive battery of memory tests was administered on three occasions, each six weeks apart. In addition, proton magnetic resonance spectroscopy (H-1-MRS) was used to measure metabolite levels in seven voxels of interest (VOIs) (including hippocampus) before and after learning.Results: Results indicate a facilitation of new learning that was evident six weeks after rote learning ceased. This facilitation occurred for verbal/episodic material only, and was mirrored by a metabolic change in left posterior hippocampus, specifically an increase in NAA/(Cr+Cho) ratio.Conclusion: Results suggest that repeated activation of memory structures facilitates anamnesis and may promote neuronal plasticity in the ageing brain, and that compliance is a key factor in such facilitation as the effect was confined to those who engaged fully with the training