bluuebunny/crossref_metadata_2025_split huggingface dataset:
Vitamin D and pneumonia in children in the high Ecuadorian Andes (639.11)
Authors: Mokhtar Rana , Holick Michael , Griffiths Jeffrey , Sempertegui Fernando , Estrella Bertha , Moore Lynn , Hamer Davidson 
Published: June 2021

Background: Recent studies have explored the relationship between vitamin D deficiency and respiratory infections. The role that vitamin D deficiency plays with acute lower respiratory infections (ALRI) is of particular importance as pneumonia causes nearly 1.3 million deaths per year in children under 5 years.Objective: To determine the association between vitamin D status and pneumonia in children aged 6‐36 months in the Ecuadorian Andes.Design: We conducted a secondary analysis of a randomized controlled trial, the Vitamin A and Zinc Prevention of Pneumonia (VAZPOP) study; a weight‐stratified, community‐based study involving children living near Quito, Ecuador who were randomized to receive vitamin A and/or zinc supplementation and followed for 48 weeks to determine the impact on episodes of pneumonia. ALRI was defined as an increased respiratory rate of 40 breaths per minute and/or lower respiratory secretions with at least one of the following: cough, fever, or chest retractions. Vitamin D deficiency was defined as serum 25(OH)D concentration <20 ng/mL and was measured using an automated immunoassay system (Immunodiagnostics Systems).Results: Of the 526 subjects who had 25(OH)D concentrations measured, 67 (13%) incident cases of pneumonia occurred over the course of 48 weeks. After controlling for treatment arm, vitamin D deficient children showed a non‐significant trend in developing pneumonia than those who were vitamin D sufficient (RR = 1.67,95%CI = 0.93‐2.98, p=0.086). Infants (<12 months) were 3.10 times more likely to develop pneumonia than children 蠅12 months (RR = 3.10, CI =1.74 ‐ 5.53, p=0.0001). Females were less likely to develop pneumonia compared to males (RR = 0.55, CI =0.31 ‐ 0.96, p=0.035).Conclusions: In Andean children, younger male children were more likely to develop an incident case of pneumonia although we found no association between vitamin D deficiency and ALRI. More research is needed to further define the association of vitamin D and pneumonia.Grant Funding Source: Supported by Sight and Life
Assessment of body composition in IBD children by bioelectrical impedance, DEXA and isotopic dilution methods (640.8)
Authors: Godin Jean‐Philippe , Ezri Jessica , Marques Vidal Pedro , Martin Francois‐Pierre , Nydegger Andreas 
Published: June 2021

Background: This study is part of a research program to characterize energy balance in children with inflammatory bowel disease (IBD). In this frame, assessment of body composition provides important information regarding disease status in children. However, body composition data are lacking for most pathological conditions and methods comparison provide a useful guide to clinicians. Aim: To determine the level of agreement between three different methods of body composition assessment among children with IBD.Method: The study was approved by the local Swiss Ethics committee. 16 IBD children (8 girls and 8 boys, mean age 14.7 ± 1.3 years) and 23 healthy children (9 girls and 14 boys, mean age 13.0 ± 2.1 years) completed the study. Fat‐free mass (FFM, in kg) was assessed by DEXA (only in IBD children), bioimpedance analysis (BIA) and double labeled water (DLW) method.Results: In IBD children, FFM (kg) was 35.4 ± 5.3 by BIA vs. 34.2 ± 5.3 by DEXA (paired t‐test: p=0.07) and 36.0 ± 5.9 by DLW (p=0.28 between BIA and isotopes; p<0.02 between isotopes and DEXA). In healthy children, FFM (kg) was 38.3 ± 10.7 by BIA, vs. 40.5 ± 12.3 by DLW (paired t‐test: p<0.01). For IBD children, regressions between BIA and DEXA showed a slope of 0.90, between DLW and DEXA a slope of 0.98 and between BIA and DLW a slope of 0.83.Conclusion: In children with IBD, assessment of FFM by BIA is a non‐invasive method and provides adequate results relative to DEXA and DLW measurements.Grant Funding Source: Supported by a Swiss grant
High‐amylose maize resistant starch 2 favorably influences body composition in healthy overweight adults (641.4)
Authors: Maziarz Mindy , Preisendanz Sara , Sherrard Melanie , Paulson Rene , Imrhan Victorine , Prasad Chandan , Juma Shanil , Vijayagopal Parakat 
Published: June 2021

As the worldwide obesity epidemic perseveres, efforts to identify ingredients that can aid in weight loss are heightened. A small reduction in fat mass can reduce chronic disease incidence and improve metabolic outcomes in overweight individuals. High‐amylose maize resistant starch 2 (HAM‐RS2) is a functional ingredient rich in fiber that may influence satiety and body composition. The aim of this study was to determine the effect of HAM‐RS2 on satiety and body composition using a randomized‐controlled, double‐blind design. Twenty healthy, overweight (BMI 蠅 27) adults (17 female, 3 male) were recruited. Participants consumed either the treatment (n = 13) with 30 g HAM‐RS2, or placebo (n = 7) with fully‐digestible starch, daily for six weeks in muffins. Subjective satiety, using a visual analogue scale, and body composition, using anthropometrics and dual‐energy x‐ray absorptiometry (DXA), were measured at baseline and week six. A decrease in waist‐to‐hip ratio (‐0.0310, P = 0.019), but increase in hip circumference (3.5146 cm, P = 0.033) occurred from baseline to week six in the HAM‐RS2 group. Reductions in trunk fat mass, android fat mass, and fasting blood glucose also resulted from HAM‐RS2 consumption. No significant changes in body composition or subjective satiety from baseline to week six were found between groups. HAM‐RS2 appears to favorably shift fat mass patterns which may influence metabolic outcomes.Grant Funding Source: Supported by the Texas Woman's University Research Enhancement Fund and Ingredion, Inc.
The effects of vitamin A and retinoic acid supplementation to neonatal rats or dietary vitamin A supplementation to lactating mothers on vitamin A metabolism and kinetics in neonatal rats (645.20)
Authors: Tan Libo , Green Michael , Ross A. 
Published: June 2021

The objective of the present study was to explore how vitamin A (VA) supplementation to neonatal rats or lactating mothers affects VA status and kinetics in neonatal rats. Rat pups received an oral dose of [3H]retinol admixed with oil (group 1; control group) or VARA (group 2) on postnatal day 4 (P4); pups in group 3 were given a VARA dose on P2 and P3 and received an oral dose of [3H]retinol admixed with oil on P4; the diet fed to mothers of pups in group 4 was switched from VA marginal to VA supplemented on the birth day of pups and pups received an oral dose of [3H]retinol admixed with oil on P4. Mothers in group 1, 2, and 3 were fed a VA marginal diet through the study. Pups (n=3/time) were sacrificed and tissues were collected at different time points up to P18. Compared with control group, the single VARA dose significantly increased retinol concentration in plasma, liver and lungs in the first 2‐4 days. Two‐time pre VARA dose dramatically increased liver and lung retinol concentration in the first 8 days and retinol concentration declined afterwards. The effects of both ways of VARA administration disappeared at the end of the study. The effect of maternal VA supplementation on increasing pups’ liver and lung total retinol was not as rapid as that of VARA, however, it increased with time till the end of the study. All three ways of VA supplementation decreased the fraction of [3H]retinol remaining in plasma and increased the fraction in liver and lungs. To conclude, high dose VARA to neonatal rats has a dramatic but transient effect, while dietary VA supplementation to lactating mothers has a gradually increasing and sustained effect on improving VA status in neonatal rats.Grant Funding Source: Supported by NIH
Impact of provitamin A biofortified maize on vitamin A status in Zambian children (646.6)
Authors: Palmer Amanda , Chileshe Justin , Schulze Kerry , Siamusantu Ward , Klemm Rolf , Molobeka Ngosa , Barffour Maxwell , Kalungwana Ng'andwe , Arguello Margia , West Keith 
Published: June 2021

Vitamin A (VA) deficiency remains a nutritional concern in Sub‐Saharan Africa. We conducted a cluster‐randomized controlled trial to test the impact of proVA biofortified maize flour consumption on VA status. All 4‐8 y old children (n=1,226) in a study area of ~400 km² in Mkushi, Zambia were enrolled and grouped by proximity into clusters of ~15‐25. We randomized clusters to: a) biofortified “orange” maize flour (n=25 clusters); b) white maize flour (n=25); or 3) non‐intervened control (n=14). Intervened clusters received 200 g maize flour, 6 d/wk for 6 mo prepared as per standardized recipes. Food packages were given in non‐intervened clusters after the trial. At baseline and follow‐up, we collected venous blood to measure serum retinol, beta‐carotene, CRP, and AGP. Groups were comparable at baseline. Although attendance did not differ (85%), median daily intake was higher in white (156 g/d) vs orange (140 g/d; providing ~75% RDA for VA) clusters. At follow‐up, serum β‐carotene was 0.3 μmol/L (95% CI: 0.2‐0.4) higher in orange clusters (p<0.001), but mean serum retinol (1.06 ± 0.43 μmol/L overall) and VA deficiency prevalence (18.6% overall; <0.7 μmol/L) did not differ by trial arm. In this marginally nourished population, regular biofortified maize flour consumption did not improve VA status.Grant Funding Source: Supported by HarvestPlus and the Canadian International Development Agency
In vitro determination of bioactive fraction of blueberry for type 2 diabetes prevention (647.17)
Authors: Kang Bouhee , Racicot Kenneth , Pilkenton Sarah , Apostolidis Emmanouil 
Published: June 2021

The present study investigates the carbohydrate hydrolysis enzyme inhibitory activity of blueberries and if this activity is proanthocaynidin (PAC) or low molecular weight phenolic (LMP) dependent. Freeze‐dried blueberry powder was extracted using 70% acetone solution (BAE) and in deionized water (BWE). Sugars were removed from both extracts using C18 cartridges. BAE resulted to higher PAC and total phenolic content (TPC), so BAE was used for the remaining experiment. LMP and PAC were separated from BAE using a LH‐20 column by washing using 30%methanol solution (LMP recovery) and eluting using 70% acetone solution (PAC recovery). PAC contents were determined as 0.86 mg/mL, 0.56 mg/g, 0.11 mg/g and 0.61 mg/mL for BAE, BWE, LMP and PAC, respectively. The TPC of BAE, BWE, LMP and PAC were determined to be 3.88 mg/mL, 2.64 mg/mL, 1.90 mg/mL and 1.85 mg/mL, respectively. Evaluation of rat α‐glucosidase inhibitory activity, revealed that LMP (IC50 0.24 mg/mL TPC basis) had the highest inhibitory activity followed by BAE (IC50 0.39 mg/mL TPC basis), PAC (IC50 0.92 mg/mL TPC basis). Evaluation of specific maltase and sucrase inhibitory activities confirmed same trend as with observed rat α‐glucosidase inhibitory activities (LMP>BAE>PAC). Our findings suggest that blueberry extract has α‐glucosidase inhibitory activity, which is low molecular weight phenolic dependent.Grant Funding Source: Supported by US Army Natick Soldier Research Engineering Center
Clinical trial for improvement in metabolic syndrome by Korean Chungkookjang (647.27)
Authors: Byun Moon‐Sun , Yu Ok‐Kyeong , Kim Hyun‐Suk , Park Tae‐Sun , Cha Youn‐Soo 
Published: June 2021

In this study, we investigated the effect of Korean trational Chungkookjang compared to placebo on variables of metabolic syndrome in overweight/obese subjects. This double‐blind randomized controlled crossover trial was conducted on 120 overweight/obese subjects; aged 19‐29 years. Each group received either 35 g of Chungkookjang (CK; n = 60) or placebo (PC; n = 60) on a regular daily basis for 12 weeks. After 12‐weeks period, the groups was crossed over. The anthropometric measures, blood pressure, glucose parameter, lipid profile, adipocytokine, and carnitine assay was determined at baseline and 12 week. Also, safety was assessded by measuring total bilirubin, alkaline phosphatase, alanine transaminase, aspartate aminotransferase, total protein, albumin, blood urea nitrogen, creatinine, and creatine kinase at baseline and 12 weeks. 24‐hour dietary recalls were collected at the baseline and at the end of the trial. Bodyweight, bodyweight gain, serum insulin , leptin level and energy intake were reduced in the CK group. These results suggested that the supplementation of Chungkookjang may contribute to the reduction of risk factor for metabolic syndrome caused by obesity.Grant Funding Source: Korean Institute of Planning & Evaluation for Technology in Food, Agriculture Forestry & Fisheries
Preventive activity of Ajuga pantantha Hand‐Mazz on reserpine‐induced experimental gastric ulcer in Kunming mice (647.8)
Authors: Li Guijie , Zhao Xin , Song Jia‐Le , Sun Peng , Qian Yu , Wang Qiang 
Published: June 2021

The aim of this study was to investigate the gastric ulcer preventive activity of aqueous extract from Ajuga pantantha Hand‐Mazz (AHMAE) on reserpine‐induced experimental gastric ulcer in Kunming mice. The mice were divided into the following five groups: normal, reserpine, 250 mg/kg and 500 mg/kg AHMAE and ranitidine. The mice were first treated with AHMAE for 28 days, and the gastric ulcer was induced by reserpine(10 mg/kg) via a intraperitoneal injection at day 29. Ranitidine (50 mg/kg) used as a positive control. Following intraperitoneal injection 24 h later, the area of gastric ulcer, gastric juice volume, gastric juice acidity, serum levels of MOT, SS, SP and VIP, serum pro‐inflammatory cytokines (IL‐6, IL‐12, TNF‐α and IFN‐γ), iNOS and COX‐2 gene expressions were analyzed. Following pretreatment with 250 and 500 mg/kg AHMAE significantly reduced the reserpine‐induced gastric ulceration. AHMAE also increased the serum SS and VIP and decreased the MOT and SP levels in serum. In addition, AHMAE significantly reduced the serum levels of pro‐inflammatory cytokines of IL‐6, 12, TNF‐α and IFN‐γ compared to control group. AHMAE also decreased the expression of iNOS and COX‐2. These results suggest that AHMAE showed a good gastric ulcer preventive effect.Grant Funding Source: Supported by the China Scholarship Council (No. [2012]5030) for fellowship
The role of frataxin in doxorubicin‐mediated cardiac hypertrophy (648.6)
Authors: Mouli Shravanthi , Nanayakkara Gayani , Fu Rain , Berlin Avery , Alasmari Abdul , Arnold Robert , Amin Rajesh 
Published: June 2021

Heart failure is the major fatal adverse effect associated with cancer chemotherapeutic, doxorubicin (DOX). We and others have found that the progression towards DOX mediated heart failure involves myocardial energy dysregulation and the development of cardiac hypertrophy. Hypothesis: We hypothesize that Frataxin (FXN) is a key player in the development and progression of DOX mediated cardiac hypertrophy. Results: Recently, we observed that DOX (2µM) treatment in H9C2 cardiomyocytes results in the reduction of the active version of the mitochondrial protein FXN which is a major player in the iron sulfur cluster biogenesis. This deficiency in the active form of FXN resulted in an increase in mitochondrial iron accumulation and consequent reduction in activities of aconitase and the electron transferring complexes in mitochondria thus greatly affecting oxidative phosphorylation leading to reduced measured levels of ATP. Further the increase in mitochondrial iron accumulation lead to an increase in production of mitochondrial reactive oxygen species (ROS) and oxidative stress and helps further explain the subsequent cardiac hypertrophy. In order to verify that restoration of FXN could prevent against myocardial energy dysregulation and cardiac hypertrophy, we created FXN over expressing and knock out cell lines and found that over expression promoted iron homeostasis in the mitochondria which lead to a significant improvement in oxidative phosphorylation, substantial decrease in ROS production in the mitochondria and protected against the development of DOX mediated cardiac hypertrophy. Conclusion: Over expression of FXN in the mitochondria is protective against DOX mediated myocardial energy dysregulation and subsequent cardiac hypertrophy.Grant Funding Source: Auburn university Internal grant program
Effects of LY294002 on the dystrophin expression in myocardium in mice submitted to cecal ligation and puncture (648.9)
Authors: Campos Pulici Erica , Celes Mara , Figueiredo Maria , Freitas Ana , Ramos Simone 
Published: June 2021

The cell signaling pathways related to PI3K play an important role in the pathogenesis of diseases with inflammatory component, such as cancer, myocardial infarction, atherosclerosis, ischemia‐reperfusion injury and sepsis. Recent evidence indicates that the PI3K/Akt signaling pathway may represent a compensatory mechanism in order to limit the pro‐apoptotic and pro‐inflammatory events in response to sepsis. This pathway has also been reported as a regulator of cardiomyocyte contractility, which could be related to expression of the structural glycoproteins, mainly dystrophin that confers structural stability to the myofiber sarcolemma and transmits force between sarcomeres and cell membrane to the extracellular matrix. Severe sepsis was induced by cecal ligation and puncture (CLP) in mice and the LY294002 (5mg/kg) was used 1 hour before surgery to inhibit the PI3K/Akt signaling. The survival rate was higher in CLP plus LY294002 group as compared to only CLP and controls. Histopathologycal analysis showed foci of disorganized miofibrils and increased membrane permeability, more evident in CLP plus LY294002 group as compared to only CLP and controls. We observed decreased myocardial dystrophin expression in septic mice as compared to controls, but this dysthophin loss was more pronounced in myocardium from septic mice treated with LY294002. The initial evidences suggest that PI3K/AKT signaling may be involved in these myocardial structural changes and could be implicated in sepsis‐induced cardiac depression and represents an innovative approach to study the intrinsic mechanism of cardiac abnormalities caused by sepsis, which can provide highly significant contribution in this specific area of knowledge.Grant Funding Source: FAPESP
Friedreich ataxia: metal dysmetabolism in dorsal root ganglia (651.1)
Authors: Mazurkiewicz Joseph , Ramirez R Liane , Koeppen Arnulf 
Published: June 2021

Friedreich ataxia (FA) is caused by an inherited deficiency of frataxin, a small nuclear genome‐encoded mitochondrial protein and leads to Fe related mitochondrial dysfunction. Atrophy of large dorsal root ganglion (DRG) neurons, hyperplasia of satellite cells, and absorption of dying neurons into residual nodules are hallmarks of FA. Dysregulation of antioxidant defenses due to over production of reactive oxygen species by transition metals (e.g. Zn and Fe) has been implicated in FA pathology. Tissue levels of Fe and Zn in normal and FA DRG did not differ significantly, however, the Zn level found, ~90.24 μM, is much higher than needed for normal function of Zn‐dependent proteins and the disturbance of Zn buffering could lead to mitochondrial damage and cell death. The Zn‐transporter, Zip14 (neurons & satellite cells), metallothionein MT1/2 (Zn; satellite cells), metallothionein 3, MT3 (Zn; neurons), and ferritin (Fe) were used as surrogates for Zn and Fe. Major shifts in Zip14 and MT1/2 immunofluorescence between neurons and satellite cells in FA DRG suggests that the metals released from dying neurons move into the proliferating satellite cells. In contrast to Zn, sequestration of Fe in satellite cells may represent a protective mechanism. Changes in the expression and cellular localization of metal handling proteins link metal dysmetabolism with the pathogenesis of the DRG lesion in FA.Grant Funding Source: Supported by grant from National Institutes of Health (R01‐NS069454), Bethesda, MD, USA
Traumatic brain injury augments disease pathology in a mouse model of amyotrophic lateral sclerosis and wild type mice (651.11)
Authors: Evans Teresa , Jaramillo Carlos , Van Remmen Holly 
Published: June 2021

Traumatic Brain Injury (TBI) is a known risk factor for ALS. The goal of this study is to elucidate the mechanism linking TBI to motor neuron disease, by testing the hypothesis that TBI will accelerate disease progression in an animal model of ALS. We used a well‐characterized mouse model of familial ALS (G93A SOD1) to study the effect of TBI on ALS progression. Mice were subjected to a closed head traumatic brain injury and magnetic resonance imaging (MRI) was used 3 days after injury to characterize structural central nervous system pathology and the severity of brain injury. Histological techniques showed astrocyte infiltration (GFAP) and edema (Nissl) following mild TBI in brain and spinal cord of wildtype (WT) and transgenic mice (TG). Our results indicate that TBI leads to early reductions in grip strength and rotarod performance. Further, muscle denervation is potentiated as is shown via electromyography abnormalities. We have also characterized the effect of TBI on disease related weight loss and overall disease score in G93A mice. Our results are the first to show that TBI, in an animal model of ALS, results in significantly increased muscle denervation and brain and spinal cord pathology.Grant Funding Source: This work is supported by an individual NRSA fellowship grant, 1F31NS080508‐01
Effects of HIV‐1 Tat and morphine on the biophysical properties of sodium channels (653.5)
Authors: Fitting Sylvia , Ngwainmbi Joy , Knapp Pamela , Hauser Kurt , Akbarali Hamid 
Published: June 2021

HIV‐infection continues to be a major clinical manifestation in the combination antiretroviral therapy era (cART), that is enhanced in opioid‐drug abusers. The gastrointestinal (GI) mucosa plays a major role in HIV‐infection as HIV is mostly transmitted across mucosal surfaces. The enteric nervous system (ENS) controls several GI processes including motility and secretion which are specifically affected in HIV‐infected patients. Opioids directly affect the ENS, causing severe constipation. Because the virus does not infect neurons, it is suggested that viral toxins, such as Tat, modulate neuronal function in HIV‐1‐infected patients. Tat has been shown to increase neuronal excitability but not much is known about effects of Tat on enteric neurons in combination with drug abuse. Recent experimental studies in our lab have shown that Tat increases enteric neuronal excitability by shifting the voltage‐dependence of activation of sodium channels to more negative potentials. In contrast, morphine alone decreases the availability of sodium channels in enteric neurons reducing excitability. Voltage gated sodium channels (VGSCs) are responsible for the generation and propagation of action potentials in neurons. In order to determine the effects of Tat (100 nM) in combination with morphine (0.3µM, 3µM) on the voltage dependence of steady‐state activation/ inactivation of sodium channels, we used a double‐pulse protocol in which a variable conditioning pulse was applied from −100mV to +50mV in 10mV steps for 50 ms followed by a test pulse. In Tat‐treated neurons, the sensitivity to morphine was significantly enhanced. The V0.5 for steady‐state inactivation was shifted in Tat‐treated neurons at 0.3 uM morphine with 50% decrease in maximal availability at ‐100 mV. Morphine did not alter the steady‐state activation. Taken together, data suggest that Tat increases the sensitivity to morphine in enteric neurons that may exacerbate the deleterious effects of morphine on GI motility.Grant Funding Source: Supported by NIDA R01 DA018633, K02 DA027374, K99 DA033878, DK046367.