Food Insecurity for the Immigrant Population During the Novel Coronavirus-19

The novel Coronavisur-19 (COVID-19) has caused s widespread loss of life in the United States and globally and wrought enormous changes to our culture and lives. COVID-19 also has caused and intensified food insecurity, especially for immigrants. The pandemic has made visible and exacerbated longstanding problems of food insecurity and hunger in America. This paper suggests several approaches to mitigating food insecurity. Focusing on the immigrant community, the author argues that we can reduce hunger by reexamining and reinvigorating existing community resources and practical strategies, including neighborhood ethnic food stores, community gardens, advocacy, and outreach programs; and by enlisting specific local, state, and Federal support

Sweeteners Unproven in Fight Against Diabetes

Medical and dietetic students often co-author a column for the Daily Reflector under Dr. Kolasa's byline. The students research the topic a reader or patient has asked. Dr. Kolasa reviews their draft for technical accuracy, patient friendly language, people first language. She fact checks the study or other evidence-based reference the student provides. If a physician review is appropriate, Dr. Kolasa requests a colleague from ECU physicians to review the article. The final draft is submitted to the Reflector with the editor having the final say. The headline is written by the Reflector headline writer. The food and nutrition column has run weekly since 1987. Starting in 2020, in addition to the Daily Reflector, the article is published in daily and weekly papers owned by the Adams Publishing Group East (https://adamspg.com)This is a weekly Q and A newspaper column under the byline of Dr. Kathy Kolasa. Today's column is discussing the use of sweetners to lower calorie intake compared to sweet and unsweetened alternative beverages in context of diabetes.non

The Influence of Education on the Nutritional Knowledge of Certified Fitness Professionals

International Journal of Exercise Science 14(4): 239-249, 2021. The American Fitness Industry has seen progressive success with recent increases in facility memberships and annual revenues of fitness centers. The number of fitness trainers and instructors in the United States has persisted this growth and is projected to grow over the next decade. However, only a few known studies have investigated the nutritional education of fitness professionals. This preliminary study explores the education and knowledge among certified fitness professions (CFPs) in the United States. A cross-sectional, descriptive survey design was utilized with a convenience sample of 120 female participants from the United States who were associated with a major fitness newsletter. The average age of the participants was 48.51 years (SD 12), and they had 14.85 years of experience (SD 10.16) and worked an average of 22.04 hours per week (SD 16.78). Most of the participants had some kind of college degree (96.2%) and held a group fitness certification (76.6%) or personal training certification (47.5%). Those with a nutrition certification were found to have significantly higher nutrition knowledge test scores on the 21 question test (18.2 ± 2.0 correct to 17.1 ± 1.9, p=0.04). Additionally, it is revealed that CFPs use the internet as a primary source for nutritional information and was the most frequently used source of nutrition information accessed. This pilot study suggests a more in-depth study would be beneficial to solidify the current results and could allow for more investigation into whether or not completion of nutrition coursework within formal earned degrees by CFPs positively influences their nutritional knowledge

An in vivo root hair assay for determining rates of apoptotic-like programmed cell death in plants

In Arabidopsis thaliana we demonstrate that dying root hairs provide an easy and rapid in vivo model for the morphological identification of apoptotic-like programmed cell death (AL-PCD) in plants. The model described here is transferable between species, can be used to investigate rates of AL-PCD in response to various treatments and to identify modulation of AL-PCD rates in mutant/transgenic plant lines facilitating rapid screening of mutant populations in order to identify genes involved in AL-PCD regulation

Tissue-specific regulation of ACE/ACE2 and AT 1 /AT 2 receptor gene expression by oestrogen in apolipoprotein E/oestrogen receptor-α knock-out mice: Oestrogen regulation of ACE/ACE2 and AT1/AT2

ACE and ACE2 and the AT1 and AT2 receptors are pivotal points of regulation in the renin-angiotensin system. ACE and ACE2 are key enzymes in the formation and degradation of Ang II and Ang-(1-7). Ang II acts at either the AT1 or the AT2 receptor to mediate opposing actions of vasoconstriction/vasodilation. While it is known that estrogen (E2) acts to down-regulate ACE and the AT1 receptors, its regulation of ACE2 and the AT2 receptor and the involvement of a specific estrogen receptor subtype are unknown. To investigate the role of estrogen receptor-α (ERα) in estrogen’s regulation of ACE/ACE2 and AT1/AT2 mRNAs in lung and kidney, ovariectomized female mice lacking apolipoprotein E (ee) with the ERα (AAee) or without the ERα (ααee) were treated with 17-β estradiol (6 µg/day) or placebo for 3 months. ACE,ACE2 and AT1/AT2 receptor mRNAs were measured using reverse transcriptase, real-time polymerase chain reaction (RT/RT-PCR). In the kidney, 17-β estradiol showed 1.7 fold down-regulation of ACE mRNA in AAee mice, with 2.1-fold up-regulation of ACE mRNA in ααee mice. 17-β estradiol showed 1.5 and 1.8 fold down-regulation of ACE2 and AT1 receptor mRNA in AAee mice; this regulation was lost in ααee mice. 17-β estradiol showed marked (81-fold) up-regulation of the AT2 receptor mRNA in AAee mice. In the lung 17-β estradiol treatment had no effect on AT1 receptor mRNA in AAee mice, but resulted in a 1.5-fold decreased regulation of AT1 mRNA in ααee. There was no significant interaction of estrogen with ER in the lung for ACE, ACE2, and AT2 receptor genes. These studies reveal tissue specific regulation by 17-β estradiol of ACE/ACE2 and AT1/AT2 receptor genes with the ERα receptor primarily responsible for the regulation of kidney ACE2 , AT1 receptor, and AT2 receptor genes

The Tetraspanin Protein Peripherin-2 Forms a Complex with Melanoregulin, a Putative Membrane Fusion Regulator

Peripherin-2, the product of the rds gene, is a tetraspanin protein. In this study, we show that peripherin-2 forms a complex with melanoregulin (MREG), the product of the Mreg locus. Genetic studies suggest that MREG is involved in organelle biogenesis. In this study, we explore the role of this protein in processes associated with the formation of disk membranes, specialized organelles of photoreceptor rod cells. MREG antibodies were generated and found to be immunoreactive with a 28 kDa protein in retinal extracts, bovine OS, ARPE-19 cells, and rat RPE. MREG colocalized with peripherin-2 in WT (CB6F1/J) and in rds+/- retinas. Western blots of serial tangential sections confirmed the close association of these two proteins within the IS and basal outer segment of rods. Immunoprecipitation (IP) of OS extracts showed formation of a complex between MREG and peripherin-2-ROM-1 hetero-oligomers. This interaction was confirmed with pulldown analyses in which the GST-PerCter protein selectively pulled down His-MREG and His-MREG selectively pulled down PerCter. Biacore analysis using peptide inhibitors and per-2 truncation mutant studies allowed us to map the MREG binding site on per-2 to the last five residues of the C-terminus (Gln341-Gly346), and kinetic data predicted a KD of 80 nM for PerCter-MREG binding. Finally, the effect of MREG on photoreceptor specific membrane fusion was assayed using a disk-plasma membrane cell free assay. Preincubation of target membranes with MREG resulted in a dose-dependent inhibition of fusion with an IC50 in the submicromolar range. Collectively, these results suggest that this newly identified protein regulates peripherin-2 function. © 2007 American Chemical Society

The impact of the metabotropic glutamate receptor and other gene family interaction networks on autism.

International audienceAlthough multiple reports show that defective genetic networks underlie the aetiology of autism, few have translated into pharmacotherapeutic opportunities. Since drugs compete with endogenous small molecules for protein binding, many successful drugs target large gene families with multiple drug binding sites. Here we search for defective gene family interaction networks (GFINs) in 6,742 patients with the ASDs relative to 12,544 neurologically normal controls, to find potentially druggable genetic targets. We find significant enrichment of structural defects (P≤2.40E-09, 1.8-fold enrichment) in the metabotropic glutamate receptor (GRM) GFIN, previously observed to impact attention deficit hyperactivity disorder (ADHD) and schizophrenia. Also, the MXD-MYC-MAX network of genes, previously implicated in cancer, is significantly enriched (P≤3.83E-23, 2.5-fold enrichment), as is the calmodulin 1 (CALM1) gene interaction network (P≤4.16E-04, 14.4-fold enrichment), which regulates voltage-independent calcium-activated action potentials at the neuronal synapse. We find that multiple defective gene family interactions underlie autism, presenting new translational opportunities to explore for therapeutic interventions