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Food allergies pose a significant health risk, affecting millions of Americans, with symptoms ranging from mild discomfort to life-threatening anaphylaxis. Likewise, autoimmune diseases, where the immune system attacks healthy tissues, encompass a wide range of conditions, each with distinct symptoms and impacts on various organs. Through an analysis of Single Nucleotide Polymorphisms (SNPs), this research explores associations between specific genetic markers and phenotypic outcomes related to allergies and autoimmune diseases. Utilizing data from the genetic testing service 23andMe, this study investigated how genetic makeup may be related to individual responses to food, shedding light on underlying molecular mechanisms. Results demonstrate significant associations between certain SNPs and disease outcomes, highlighting the potential for personalized interventions in managing allergies and autoimmune disorders. This research contributes to a deeper understanding of personalized nutrition and may pave the way for novel approaches to disease prevention and management.

Continual advances in our understanding of the human genome have led to exponential increases in known single nucleotide variants. The characterization of each of the variants lags behind. For researchers needing to study a single gene, or multiple genes in a pathway, there must be ways to narrow down pathogenic variants from those that are silent or pose less pathogenicity. In this study, we use the NHLH2 gene which encodes the nescient helix-loop-helix 2 (Nhlh2) transcription factor in a systematic analysis of all missense mutations to date in the gene. The NHLH2 gene was first described in 1992. Knockout mice created in 1997 indicated a role for this protein in body weight control, puberty, and fertility, as well as the motivation for sex and exercise. Only recently have human carriers of NHLH2 missense variants been characterized. Over 300 missense variants for the NHLH2 gene are listed in the NCBI single nucleotide polymorphism database (dbSNP). Using in silico tools, predicted pathogenicity of the variants narrowed the missense variants to 37 which were predicted to affect NHLH2 function. These 37 variants cluster around the basic-helix-loop-helix and DNA binding domains of the transcription factor, and further analysis using in silico tools provided 21 SNV resulting in 22 amino acid changes for future wet lab analysis. The tools used, findings, and predictions for the variants are discussed considering the known function of the NHLH2 transcription factor. Overall use of these in silico tools and analysis of these data contribute to our knowledge of a protein which is both involved in the human genetic syndrome, Prader–Willi syndrome, and in controlling genes involved in body weight control, fertility, puberty, and behavior in the general population, and may provide a systematic methodology for others to characterize variants for their gene of interest.

Non-coding RNAs (ncRNAs) are, arguably, the enigma of the RNA transcriptome. Even though there are more annotated ncRNAs (25,967) compared to mRNAs (19,827), we know far less about each of the genes that produce ncRNA, especially in terms of their regulation, molecular functions, and interactions. Further, we are only beginning to understand the role of differential regulation or function of ncRNAs caused by genetic and epigenetic perturbations, such as single nucleotide variants (SNV), deletions, insertions, and histone/DNA modifications. The 22 papers in this Special Issue describe the emerging roles of ncRNAs in neurological, cardiovascular, immune, and hepatic systems, to name a few, as well as in diseases such as cancer, Prader–Willi Syndrome, cardiac arrhythmias, and diabetes. As we begin to understand the function and regulation of this class of RNAs, strategies targeting ncRNAs could lead to improved therapeutic interventions for some conditions.

In the spring semester of 2020, the COVID-19 pandemic led to an unprecedented shift from face-to-face learning to an instantaneous online learning environment. At the time, the department of Human Nutrition, Foods, and Exercise (HNFE) at Virginia Tech had few online class offerings. Twenty-nine Spring 2020 HNFE classes were transitioned from traditional face-to-face offerings to online delivery models. Many members of the HNFE faculty have strong pedagogical training, but the immediate pedagogical shift in the middle of the semester gave little time for adequate course design geared toward online learning. As such, the purpose of this study was to evaluate student perceptions of the transition to online learning. A departmental survey employing quantitative and qualitative questions was used to assess students’ learning experiences in the spring of 2020 and then re-employed at the conclusion of the Fall 2020 semester to re-assess students’ online course experience and identify if the department was improving in online course delivery. An additional component of the survey specifically evaluated students’ self-perceived motivation for learning. Examples of educational and logistical strategies in online learning environments implemented by instructors and findings of students’ experiences from both surveys will be shared.

Prader–Willi Syndrome (PWS) is a human genetic condition that affects up to 1 in 10,000 live births. Affected infants present with hypotonia and developmental delay. Hyperphagia and increasing body weight follow unless drastic calorie restriction is initiated. Recently, our laboratory showed that one of the genes in the deleted locus causative for PWS, Snord116, maintains increased expression of hypothalamic Nhlh2, a basic helix–loop–helix transcription factor. We have previously also shown that obese mice with a deletion of Nhlh2 respond to a conjugated linoleic acid (CLA) diet with weight and fat loss. In this study, we investigated whether mice with a paternal deletion of Snord116 (Snord116m+/p−) would respond similarly. We found that while Snord116m+/p− mice and mice with a deletion of both Snord116 alleles were not significantly obese on a high-fat diet, they did lose body weight and fat on a high-fat/CLA diet, suggesting that the genotype did not interfere with CLA actions. There were no changes in food intake or metabolic rate, and only moderate differences in exercise performance. RNA-seq and microbiome analyses identified hypothalamic mRNAs, and differentially populated gut bacteria, that support future mechanistic analyses. CLA may be useful as a food additive to reduce obesity in humans with PWS.

Prader–Willi Syndrome (PWS) is a human genetic condition that affects up to 1 in 10,000 live births. Affected infants present with hypotonia and developmental delay. Hyperphagia and increasing body weight follow unless drastic calorie restriction is initiated. Recently, our laboratory showed that one of the genes in the deleted locus causative for PWS, Snord116, maintains increased expression of hypothalamic Nhlh2, a basic helix–loop–helix transcription factor. We have previously also shown that obese mice with a deletion of Nhlh2 respond to a conjugated linoleic acid (CLA) diet with weight and fat loss. In this study, we investigated whether mice with a paternal deletion of Snord116 (Snord116m+/p−) would respond similarly. We found that while Snord116m+/p− mice and mice with a deletion of both Snord116 alleles were not significantly obese on a high-fat diet, they did lose body weight and fat on a high-fat/CLA diet, suggesting that the genotype did not interfere with CLA actions. There were no changes in food intake or metabolic rate, and only moderate differences in exercise performance. RNA-seq and microbiome analyses identified hypothalamic mRNAs, and differentially populated gut bacteria, that support future mechanistic analyses. CLA may be useful as a food additive to reduce obesity in humans with PWS.

This study aimed to determine if an acute bout of exercise could improve academic performance when compared to sedentary behavior within a 2-hour window before a college exam. The participants of this study completed two bouts of an intervention on two separate occasions, exercise and sedentary, then completed each of the two class exams, followed by a short survey to gain insight on motivation and anxiety. A 2-way ANOVA was used to determine a time or group effect as this study was completed over a 15-week semester and found no significant difference between the group’s exam scores over time, as well as no group effect of the acute bout of exercise on their exam performance. Pre- and post-surveys, as well as post-exam surveys collected data relating to IPAQ, MSLQ, and GRIT which found significant correlations between IPAQ and perceived exam preparedness with P=0.041. As expected in academia, each exam’s scores were positively related to final course grades with P=0.0275 on exam 1 and P=0.0179 on exam 2. Finally, a P=0.048 was found between final course grades and scores from the extrinsic motivations section of the MSLQ on the post-study survey. Results and lessons learned from this pilot study should be used towards creating a larger-scale study in the future.

The Small Nucleolar Host Gene 14 (SNHG14) is a host gene for small non-coding RNAs, including the SNORD116 small nucleolar C/D box RNA encoding locus. Large deletions of the SNHG14 locus, as well as microdeletions of the SNORD116 locus, lead to the neurodevelopmental genetic disorder Prader–Willi syndrome. This review will focus on the SNHG14 gene, its expression patterns, its role in human cancer, and the possibility that single nucleotide variants within the locus contribute to human phenotypes in the general population. This review will also include new in silico data analyses of the SNHG14 locus and new in situ RNA expression patterns of the Snhg14 RNA in mouse midbrain and hindbrain regions.

FADS1 is a key regulator of fatty acid metabolism with important implications for athlete health and performance. Mutations in the FADS1 gene have been linked to a variety of adverse health conditions, in addition to alterations in biochemical levels of fatty acids. Polyunsaturated fatty acids, including omega-3 and omega-6 fatty acids, are associated with rates of inflammation, immune function, and brain health in athletes. The purpose of this study was to explore the relationship between genetic variability, specifically in the FADS1 gene, and fatty acid metabolism in an athletic population. Methods: 20 collegiate football players were recruited for this study. Saliva samples were collected for the purpose of obtaining genetic information. Serum samples for ALA, AA, EPA, and DHA were collected to measure omega-3 and omega-6 fatty acid levels. Genotypes and serum measurements were compared using 3x3 Fisher Exact tests, and the online software PROVEAN was used to identify potential novel variants in the FADS1 gene. Results of this exploratory study suggest the minor allele for 9 variants in the FADS1 gene decrease baseline serum levels of EPA. These results suggest that genetic data may be useful in assessing individual athlete risk for n-3 PUFA deficiency and associated health consequences. Subsequently, this may allow athletes and sports practitioners to make better informed decisions about individual intake and supplementation of n-3 PUFAs, specifically, EPA and DHA.

The smallest genomic region causing Prader-Willi Syndrome (PWS) deletes the non-coding RNA SNORD116 cluster; however, the function of SNORD116 remains a mystery. Previous work in the field revealed the tantalizing possibility that expression of NHLH2, a gene previously implicated in both obesity and hypogonadism, was downregulated in PWS patients and differentiated stem cells. In silico RNA: RNA modeling identified several potential interaction domains between SNORD116 and NHLH2 mRNA. One of these interaction domains was highly conserved in most vertebrate NHLH2 mRNAs examined. A construct containing the Nhlh2 mRNA, including its 3'-UTR, linked to a c-myc tag was transfected into a hypothalamic neuron cell line in the presence and absence of exogenously-expressed Snord116. Nhlh2 mRNA expression was upregulated in the presence of Snord116 dependent on the length and type of 3'UTR used on the construct. Furthermore, use of actinomycin D to stop new transcription in N29/2 cells demonstrated that the upregulation occurred through increased stability of the Nhlh2 mRNA in the 45 minutes immediately following transcription. In silico modeling also revealed that a single nucleotide variant (SNV) in the NHLH2 mRNA could reduce the predicted interaction strength of the NHLH2:SNORD116 diad. Indeed, use of an Nhlh2 mRNA construct containing this SNV significantly reduces the ability of Snord116 to increase Nhlh2 mRNA levels. For the first time, these data identify a motif and mechanism for SNORD116-mediated regulation of NHLH2, clarifying the mechanism by which deletion of the SNORD116 snoRNAs locus leads to PWS phenotypes.

For K-12 students, obesity has been linked to student educational achievements. The study objective was to determine whether academic performance in university students is correlated with BMI. Students from two consecutive academic years (Jan-May 2013 and Jan-May 2014) were given an optional class survey in May, as extra credit. Of the 452 students that completed the survey, 204 females and 75 males (N = 279; 73% female and 27% male) consented to participate in the study. The number of correct answers to problem-solving questions (PSQs) and the overall final grade for the class were compared to the calculated BMI using linear regression with a Pearson's R correlation and unpaired t-tests. BMI was significantly negatively correlated with student's final grades (P = 0.001 Pearson's r = - 0.190) and PSQs were positively correlated with final grades (P < 0.001; Pearson's r = 0.357). Our findings show a correlation between healthy body weight and improved academic performance. Further, the data suggest that future research in the area of body weight, diet, and exercise and any correlations of these with academic performance in college students are warranted.

The SNORD116 small nucleolar RNA locus (SNORD116@) is contained within the long noncoding RNA host gene SNHG14 on human chromosome 15q11-q13. The SNORD116 locus is a cluster of 28 or more small nucleolar (sno) RNAs; C/D box (SNORDs). Individual RNAs within the cluster are tandem, highly similar sequences, referred to as SNORD116-1, SNORD116-2, etc., with the entire set referred to as SNORD116@. There are also related SNORD116 loci on other chromosomes, and these additional loci are conserved among primates. Inherited chromosomal 15q11-q13 deletions, encompassing the SNORD116@ locus, are causative for the paternally-inherited/maternally-imprinted genetic condition, Prader–Willi syndrome (PWS). Using in silico tools, along with molecular-based and sequenced-based confirmation, phylogenetic analysis of the SNORD116@ locus was performed. The consensus sequence for the SNORD116@ snoRNAs from various species was determined both for all the SNORD116 snoRNAs, as well as those grouped using sequence and location according to a human grouping convention. The implications of these findings are put in perspective for studying SNORD116 in patients with inherited Prader–Willi syndrome, as well as model organisms.