bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sustained Resveratrol infusion increases renal blood flow without changing glomerular filtration rate in normal rat (692.1)
Authors: Gordish Kevin , Beierwaltes Wiliam 
Published: June 2021

The polyphenol resveratrol has cardiovascular benefits, but it’s effect on renal hemodynamics and glomerular filtration rate (GFR) remain unknown. Resveratrol vasodilates by increasing nitric oxide (NO), may inhibit reactive oxygen species (ROS), and prevent ROS depletion of NO. We found an acute bolus of resveratrol transiently increased renal blood flow (RBF) and decreased renal vascular resistance (RVR). We hypothesized a sustained infusion of resveratrol may increase RBF, and therefore GFR. We infused vehicle for 30 minutes followed by resveratrol infusion (30 minutes) at of 0, 0.5, or 1.0 mg/min. We measured RBF, calculated RVR and measured GFR with FITC‐inulin. 1.0 mg/min resveratrol infusion increased RBF by 15%, from 7.17±0.40 to 8.25±0.40 ml/min/gkw (p<0.01, n=7). RVR decreased from 13.61±0.85 to 11.81±1.01 ARU (p<0.04). GFR remained unchanged (1.61±0.17 vs. 1.68±0.20 mg/min/gkw, respectively). In separate experiments, control RBF was unchanged with 0.5 mg/min resveratrol (7.69±0.84 vs. 7.88±0.94 ml/min/gkw, n=9). RVR was also unaffected. Control GFR was 0.98±13 ml/min/gkw remained unchanged by resveratrol (1.12±0.22 ml/min/gkw). We conclude that a constant infusion of resveratrol induced a significant increase in RBF and decreased RVR while not changing GFR, suggesting uniform dilator effects on both afferent and efferent resistance vessels.Grant Funding Source: supported by NIH 5P01HL090550‐04
Increased oxidative damage in the plasma of adult type 2 diabetics with poor glycemic control (693.7)
Authors: Platat Carine , Habib Hosam , Souka Usama , AlMaqbali Fatma , Kamal Hina , Ibrahim Wissam , Baynouna Latifa , Ali Habiba 
Published: June 2021

Increased oxidative damage in the plasma of adult Type 2 diabetics with poor glycemic control Increasing evidence associates oxidative stress with the pathogenesis of Type 2 Diabetes (T2DM). Nonetheless, the available data related to oxidative stress and its relationships with glycemic status among T2DM patients are scarce and contradictory.Our goal was to investigate the relationships of metabolic control of T2DM with oxidative damage and antioxidant status.T2DM Emirati adults (n=187), participating in the Skills for Change randomized intervention trial and recruited from seven different ambulatory health care centers in Al Ain, United Arab Emirates, were considered. 24 h‐recall was collected. Anthropometry and HbA1c were assessed. Aantioxidant status markers were measured: Vitamin C, ABTS, Ferric Reducing Ability of Plasma (FRAP) and Glutathione (GSH). After stratification on HbA1c and age, oxidative damage (Malonaldehyde (MDA), protein carbonyls) were assessed in a sub‐sample (n=47).Means ± s.d. or percentages were calculated as appropriate. General linear model was used with adjustment for age, body mass index, food groups’ consumption (fruits, vegetables meat/beans, dairy), fat and total daily energy intakes.In the whole sample, mean age was 53.46±9.36 years, mean HbA1c was 7.69±1.54 %. A majority (86.50%) of patients was taking oral medication. Mean values for vitamin C, ABTS, FRAP and GSH were 0.09±0.07 g/L, 0.10±0.04 g /L, 1.00±0.46 g/L and 0.13±0.03 g/L, respectively. In the sub‐sample, MDA and protein carbonyls were 12.67±3.44 µmol/L and 0.29 nmol/L, respectively. None of the markers of antioxidant status were significantly related to HbA1c. MDA and protein carbonyls were strongly positively associated with HbA1c (p=0.02, 0.01, respectively).In this work, poor glycemic control is strongly positively associated with oxidative damage in adults with T2DM, suggesting that oxidative stress is closely intertwined with this disease.Grant Funding Source: Supported by Sheikh Hamdan Award
Nitrite supplementation improves arterial mitochondrial health in old mice (698.5)
Authors: Sindler Amy , Johnson Lawrence , de Picciotto Natalie , Ahsan Sanjana , Weber Stewart , Seals Douglas , Gioscia‐Ryan Rachel 
Published: June 2021

Age‐related declines in endothelial‐dependent dilation (EDD) are mediated in part by excessive mitochondrial (mito) reactive oxygen species (mtROS) production. Since nitrite improves vascular function with aging and enhances mito health, we hypothesized that nitrite supplementation (drinking water, 50 mg/L, 8 w) would improve arterial mito health in old mice. Old (O; 27 mo, n = 9) C57 male mice had lower ex vivo carotid artery EDD vs. young (Y; 6 mo, n = 9) (56 ± 6 vs. 84 ± 3%, p<0.05), which nitrite restored (ON; 91 ± 3%). Incubation with the mito specific antioxidant, MitoQ (1.0 mM), selectively improved EDD in O (85 ± 4%), but had no effect in Y or ON. Increased mtROS challenge with rotenone (0.5 uM) further impaired EDD in O (35 ± 6%) while Y and ON were protected. Consistent with mtROS‐mediated vascular dysfunction in aging, arteries from O had reduced expression (WB) of key markers of mito health, including mito maintenance proteins (AMP‐activated protein kinase, O: 0.5 ± 0.1 vs. Y: 1.0 ± 0.2; peroxisome proliferator‐activated receptor γ coactivator 1‐α, O: 0.7 ± 0.1 vs. Y: 1.0 ± 0.1) and mito mass (complex IV, O: 0.6 ± 0.1 vs. Y: 1.0 ± 0.2; voltage‐dependent anion channel, O: 0.7 ± 0.07 vs Y: 1.0 ± 0.05, AU all p<0.05), which nitrite restored (ON: 1.7 ± 0.5; 1.9 ± 0.5; 1.8 ± 0.4; .9 ± 0.04 AU, respectively, all p<0.05 vs. O). Nitrite supplementation may reverse age‐related endothelial dysfunction in part by improving vascular mitochondrial health.Grant Funding Source: Supported by NIH AG013038 and AG000279
Influences of gender, age, and ethnicity on nitric oxide and cGMP concentrations biocaptured over acupoint/meridians: analysis in fifty‐nine human subjects (698.7)
Authors: Ma Sheng‐Xing , Li Xi‐Yan , Jiang Isabelle , Hu Jay , Lee Paul 
Published: June 2021

The purpose of this study was to determine the influence of gender, age, and race on nitric oxide (NO)‐cGMP concentrations over acupuncture points (acupoints), meridian lines between acupoints, and non‐meridian controls in healthy volunteers. A biocapture device was taped onto the skin surface along the Pericardium (PC) and Lung (LU) acupoints/meridian located on the arm, and the Bladder (BL) acupoints/meridian on the leg in 59 subjects. Total nitrate and nitrite (NOx¯) and cGMP levels in the biocaptured samples were measured using chemiluminescence and ELISA, respectively. Results show that cGMP concentrations over the PC acupoints and non‐meridian area are higher in females than males, but NO concentration over the region is modified by body weight, which contain more subjects with obesity in man. NO and cGMP levels along the BL meridian are increased in middle age/elder subjects compared to adolescent/adult subjects but not over PC regions. There was no detectable significance between NO nor cGMP concentrations among racial groups studied. Our findings suggest that different NO and cGMP levels between genders and age groups are influenced by sympathetic activity, body weight, hormones, sweat rates, and skin thickness. Enhanced NO and cGMP levels along the BL meridian and bladder dysfunction in aged subjects requires investigation.Grant Funding Source: Supported by NIH AT002478 and Oppenheimer Seed Grant to S. Ma
Chronic hypoxia promotes preferential loss of MLCK not associated with MLC in fetal lamb arteries (700.7)
Authors: Williams James , Aguilar Luisa , Pearce William 
Published: June 2021

As we have previously shown (PMID: 23325408), chronic hypoxia (CH) dramatically reduces MLCK abundance in fetal common carotid arteries without proportionate loss of contractility. The present study explores the hypothesis that CH preferentially decreases MLCK not associated with MLC and thereby preserves contractility. Common carotid arteries from term fetal sheep were mounted in a custom‐made organ bath apparatus that enabled computer controlled freezing of artery samples in 200 msec increments (PMID: 18835918). Artery segments were frozen in methacarn fixative and analyzed for MLC, S19 pMLC and MLCK by Westerns and confocal microscopy. CH reduced MLCK abundance 24‐fold, but did not significantly alter MLC abundance. Despite decreased MLCK abundance, rates of ser19 MLC phosphorylation after 1 sec electrical stimulation were unchanged in Calyculin A (10 nM) pre‐treated arteries (27.6±0.8% N, 22.4±4.9% H). Confocal microscopy revealed that colocalization of MLC with MLCK was increased more than 3‐fold in hypoxic arteries. These data indicate that hypoxic losses of MLCK are restricted to a fraction of MLCK not associated with MLC, such that the remaining MLCK is more tightly colocalized with MLC and is fully capable of phosphorylating MLC and sustaining contraction. The role of the large fraction of MLCK not colocalized with MLC is unclear, but may serve structural or other non‐enzymatic purposes.Grant Funding Source: Supported by NIH Grants HD‐31266 and NS‐076945
A microRNA cluster miR‐23/24/27 is regulated by aldosterone to alter Na+ transport in the kidney distal nephron (711.5)
Authors: Butterworth Michael , Liu Xiaoning , Edinger Robert 
Published: June 2021

The epithelial sodium channel (ENaC) is a major determinant of sodium (Na+) and water balance in the kidney. We previously reported that aldosterone (aldo) modifies expression of microRNAs (miRs) to alter target gene expression and regulate Na+ transport in principal cortical collecting duct (CCD) epithelial cells. These studies focus on 2 clusters of miRs that are significantly upregulated by aldo, and are members of the miR‐23/24/27 family. In cultured mCCD‐cl1 cells, aldo stimulation (50nM, 24hr) resulted in a ~1.7 fold increase in all family members as determined by microarray and qPCR. In vivo, these miRs were significantly increased (1.7‐3.5 fold) in isolated CCD cells from mice on low Na+ vs standard salt diets. Exogenous overexpression on the miRs, using oligonucleotide mimics, increased ENaC‐mediated Na+ transport in the mCCD cell line (44±5.9%, n=8, p<0.002), in the absence of aldo stimulation. Using our newly developed algorithm, ComiR, we predicted and verified regulation of intersectin 1&amp;2 as targets of these miR clusters, and possible mediators of ENaC regulation. These data confirm a central role for aldo‐regulated miRs in the maintenance of Na+ transport in the distal kidney nephron.Grant Funding Source: Supported by DK078917
Maturation of vascular anatomy in the zebrafish brain (726.1)
Authors: Rahmat Sulman , Gilland Edwin , Heinbockel Thomas 
Published: June 2021

Although embryonic and larval vasculature in zebrafish have been described, few studies document brain vessels beyond two weeks of development. Transgenic zebrafish, between one and twelve weeks old, expressing GFP in cranial motor neurons were injected with fluorescent vascular dye and examined with confocal angiography to demonstrate maturation of cerebral vasculature. A segmental series of hindbrain central arteries (CAs) in early larvae extend from the basilar artery, penetrate the midline of rhombomeres (r) r3‐8 and branch sparsely within the neuroepithelium before draining into laterally located veins. While hindbrain CAs in younger stages were roughly similar along the series, the r3 and r8 stems became progressively larger than the others, with more elaborate branching and increased neurovascular territorial supply. By 75 days, the r3 CA was effectively the arterial supply of the entire rostral hindbrain, including branches that supply the migrated facial motor nucleus in r7. Since small r4‐7 CAs are present in mature brains, it is likely that the increased territory of the r3 CA resulted from angiogenic sprouting of existing branches rather than capture of neighboring arterial trees by vessel fusion. In contrast, the major cerebellar, midbrain and forebrain arterial vessels supplied roughly the same neuronal territories in mature animals as in early larvae, but with greatly increased branching.Grant Funding Source: N/A
The unique developmental and aging profile of tau protein in the long‐lived naked mole‐rat brain resists Aβ toxicity (728.8)
Authors: Orr Miranda , Salinas Angelica , Buffenstein Rochelle 
Published: June 2021

Alzheimer’s disease (AD), the most prominent neurodegenerative disease, is characterized by Aß plaques, hyperphosphorylated tau, neurodegeneration and dementia. A prominent hypothesis suggests that elevated Aß peptide initiates AD pathogenesis including tau pathology. The tau protein, encoded by microtubule associated protein tau (MAPT) gene, is expressed predominantly in neuronal axons where it physiologically stabilizes microtubules (MTs). With over 20% of residues permissive to phosphorylation, tau function greatly depends on its phosphorylation state. Specifically, heavily phosphorylated tau loses MT binding affinity and coincides with neurodegeneration in AD. Unfortunately, genetically modified animal models overexpressing transgenic Aß have failed to recapitulate AD‐like tau misprocessing. To determine, instead, if endogenously expressed high levels of Aß alter tau and induce AD‐like pathology, we are studying the extremely long‐lived naked mole‐rat (NMR). NMRs, unlike mice, naturally contain measurable amounts of brain Aß. Using histological and biochemical assays, we have characterized tau protein from postnatal day 1 through 30 years of age. Remarkably, NMR brains display tau expression, phosphorylation, and splicing patterns distinct from mice and humans that seemingly enable them to cope with life‐long high levels of Aß.Grant Funding Source: Supported by: Biology of Aging Training Program 5T32AG021890
Alteration of metabolic activities by modulation of PI3K/AKT and mTOR pathways in ovarian cancer cells (766.10)
Authors: Calianese David , Cammarata Garrett , Best Charles , Wan Yinsheng 
Published: June 2021

Ovarian cancer accounts for three percent of all cancers that affect women world‐wide and it is regarded at the deadliest form of gynecological cancer. Alteration in cellular metabolism is a manifestation of cancer that typically results in a shift from oxidative phosphorylation to aerobic glycolysis. This change is defined as the Warburg Effect. In this study, we used cell culture techniques to investigate the metabolic behavior of an ovarian cancer cell line, CaOV3. We determined metabolic activity through XF Cell Mito Stress and XF Glycolysis stress tests using a Seahorse Bioscience XFe96 Analyzer. After titrations were completed for optimal cell number and concentration of Oligomycin, we pretreated CaOV3 cells with PI3K/AKT and mTOR inhibitors and repeated stress tests. We found that under the influence of Rapamycin (mTOR inhibitor) and LY294002 (PI3K/AKT inhibitor), the cells exhibited an increase in oxygen consumption by OCR (pMoles/min) and ECAR (mpH/min) analysis, suggesting an increase in capacity for cellular respiration and subsequent ATP production. Our results also indicated that Doxarubicin, a commonly applied chemotherapy agent, does not affect metabolic levels. Taken together, we conclude that in response to the inhibition of the PI3K/AKT and mTOR pathway that promotes protein synthesis and proliferation, the cancer cells attempt to combat the effects by increasing their metabolic capacity. Our data also suggest that modulation of PI3K/AKT and mTOR pathways and alteration of metabolic activities may reveal molecular targets for ovarian cancer treatment.Grant Funding Source: Supported by INBRE
Killing cancer cells with nanotechnology: the effect of CaS nanostructures on the cell replication rate and survival of human mammary adenocarcinoma cell lines (780.9)
Authors: Rivera Daniel , Carrasco Nestor , Maldonado Louis , Suarez Edu , Poventud Carlos , Marrero Carolina , Castro Miguel 
Published: June 2021

Calcium sulfide (CaS) nanostructures have the potential to play an important role as cadmium‐free nanoscaled semiconductors with applications in bioimaging, in vivo labeling, and sensing, and for drug delivery systems. The objective of this work is to establish the effect of CaS nanostructures on cell replication rate and survival of human mammary adenocarcinoma cell lines. Human adenocarcinoma cell lines are grown in eagle’s minimum essential medium (EMEM). Single doses of dispersions containing traces of CaS nanostructures were added to human mammary adenocarcinoma cell lines with a 70 % confluence. After a 24 hour period, 200,000 cancer cells were subculture in T‐75 treated flasks. The number of dead cells in the cell culture media supernatant was determined in intervals of 24 hours using a Biorad T10 cell counter. The number of dead cells in the supernatant is found to increase from 2,000 in control cell cultures to over 70,000 in cancer cell cultures exposed to a single dose of the CaS dispersion in the first 24 hours: this represents 35 % of the initial cell seeding. The number of dead cells remains in the range of 60,000 to 30,000 in measurements performed between 48 and 72 hours following the single dose of the dispersion containing the CaS nanostructures. The number of replicating cells is found to decrease in the first 72 hours and to increase thereafter. We conclude that the CaS nanostructures affect the replication rate and survival of human adenocarcinoma cells and demonstrate the role CaS nanostructures may play to treat localized cancers.Grant Funding Source: NIH NIGMS‐R25GM088023 and NIGMS‐R25GM096955
Viewers vs. doers: how watching food television and cooking frequency relate to BMI (811.21)
Authors: Pope Lizzy , Latimer Lara , Wansink Brian 
Published: June 2021

Objectives: Examine where nutritional gatekeepers obtain information about new foods, and whether information source impacts Body Mass Index (BMI), as well as whether any impact varied according to how often the participant cooked from scratch.Methods: Five hundred and one young women completed a survey assessing where they obtained information on new foods, and how often they cooked from scratch. Linear regressions were run to determine associations between information source, cooking from scratch, and BMI.Results: Obtaining information from cooking shows was positively correlated with BMI (p<0.05), whereas obtaining information from print, online, or in‐person sources was not significantly associated with BMI. An interaction between watching cooking shows and cooking from scratch was associated with higher BMI (p<0.05).Conclusions: Obtaining information about new foods from TV cooking shows appears to have a unique impact on BMI, versus obtaining information from other sources. Furthermore, watching cooking shows may have a differential effect on BMI for those who are “viewers,” in that they only watch the show, versus those who are “doers,” meaning they view and cook.
New Year’s res‐Illusions: food shopping in the New Year competes with healthy intentions (811.22)
Authors: Pope Lizzy , Hanks Andrew , Just David , Wansink Brian 
Published: June 2021

Objective: To assess holiday and post‐holiday purchasing patterns of unhealthy and healthy foods when compared to purchasing in early fall (baseline).Methods: Grocery‐purchase data were collected for 207 households from July 2010 to March 2011. Calorie data for foods purchased were extracted from online nutritional databases. The cooperating grocer’s proprietary nutrient‐rating system was used to designate “healthy,” and “unhealthy” items. Average weekly (Sunday through Saturday) expenditures and per‐serving calories for the holiday period, (Thanksgiving‐New Year’s), and the post‐holiday period (New Year’s‐March), were compared to average weekly expenditures during the baseline period (July‐Thanksgiving). Regression analysis was used to compare expenditures and calories purchased in each of the three time periods.Results: Household expenditures increased in the holiday period from baseline, with 75% of additional expenditures accounted for by less‐healthy items. Furthermore, expenditures increased by 53% in the post‐holiday period compared to the holiday period, and households purchased twice as many additional per‐serving calories in the post‐holiday period compared to the holiday period. Specifically, additional per‐serving calories from healthier foods increased 510% in the post‐holiday period compared to the holiday period, while purchasing of less healthy foods remained constant.Conclusions: Post‐holiday purchases of healthy items may have provided a “health halo” justifying purchasing of unhealthy items. Despite resolutions to eat more healthfully after New Year’s, consumers may adjust to a new “status quo” of increased unhealthy‐food purchasing during the holidays, and vicariously fulfill their New Year’s resolutions by spending more on healthy foods.Grant Funding Source: Supported By the National Institutes of Health (NIH), grant 1RC1HD063370‐01
Soy protein isolate and estradiol differ in their effects on the mammary gland of weanling male and female rats (818.1)
Authors: Ronis Martin , Miousse Isabelle , Gomez‐Acevedo Horacio , Hennings Leah , Shankar Kartik , Cleves Mario , Badger Thomas 
Published: June 2021

Isoflavones are phytochemical components of soy diets that bind weakly to estrogen receptors (ERs). To study potential estrogen‐like actions of soy in the mammary gland, we fed weanling male and female Sprague‐Dawley rats a casein diet from PND21 to PND33, the same diet substituting soy protein isolate (SPI) for casein, or the casein diet supplemented with estradiol (E2) at 10 μg/kg/day. In contrast to E2, the SPI diet induced no significant change in mammary morphology. In males, there were 34 genes for which expression changed 蠅2‐fold in the SPI group versus 509 changed significantly by E2, and 8 versus 174 genes in females. Nearly half of SPI‐responsive genes in males were also E2‐responsive, including adipogenic genes. Serum insulin was found to be decreased by SPI in males. SPI and E2 both down‐regulated the expression of ERα (Esr1) in males and females, and ERβ (Esr2) only in males. Chromatin immunoprecipitation (ChIP) revealed an increased binding of ERα to the promoter of the progesterone receptor (Pgr) and Esr1 in both SPI and E2 treated males compared to the casein group but differential recruitment of ERβ. ER promoter binding did not correlate with differences in Pgr mRNA expression. This suggests that SPI fails to recruit appropriate co‐activators at E2‐inducible genes. Our results indicate that SPI behaves like a selective estrogen receptor modulator rather than a weak estrogen in the developing mammary gland.Grant Funding Source: Supported by USDA‐ARS CRIS 6251‐51999‐007‐04S