bluuebunny/crossref_metadata_2025_split huggingface dataset:
Perceptions of Key Parental Benefits from Practices that Promote Intake of Calcium‐Rich Foods and Beverages (CRF/B) in Preadolescent Children
Authors: Wong Siew Sun , Gunther Carolyn , Reicks Marla , Richards Rickelle , Bruhn Christine M , Cluskey Mary , Misner Scottie , Watters Corilee , Bellajos Miriam 
Published: June 2021

ObjectiveExplore perceived benefits underlying parent practices that promote CRF/B intake by preadolescents (10–13y), including availability, setting rules and expectations, and role modeling.MethodsFocus groups using Nominal Group Technique with multi‐ethnic parents of preadolescents and qualitative data analysis methods.ResultsIn seven states (AZ, CA, HI, MN, OH, OR, UT), 156 parents (83% mothers; 22% African American, 20% Asian, 26% Hispanic, 27% non‐Hispanic White) completed the study. The top 3 perceived benefits were similar across parenting practices and included:

Making CRF/B Available
Rules & Expectations
Role Modeling

Child's bone/teeth health & growth
Child's general health
Child's health

Family's healthy eating habits/choices
Parent's positive emotions
Family's general health

Child's mental health & school performance
Child's current bone health
Family's dietary intake/choices

ConclusionHaving a healthy child was the primary perceived parental benefit of practices that promoted calcium intake by children. Secondary benefits were a healthy family diet and parent's positive emotions.Source of Research Support: USDA NIFA, AES & Extension at participating universities.
Developing and pre‐testing nutrition messages for Asian Indian mothers
Authors: Momin Shabnam R , Olson Beth 
Published: June 2021

Asian Americans born in the US are twice as likely to be overweight compared to those born elsewhere and newly migrating. The prevalence of childhood overweight for Asian Indians will increase as more Asian Indian children are born in the US. Childhood obesity prevention efforts often focus on parent behaviors that influence children's dietary intake and weight status. Research shows that Asian Indian mothers may need nutrition education materials developed specifically for this group. The aim of this study was to develop and pre‐test nutrition messages for Asian Indian mothers addressing eight parental food‐related behaviors likely to influence children's diet and weight status. Nutrition education messages developed by USDA were used with some adaptations and new messages were developed as needed based on the qualitative work previously completed with Asian Indian mothers. These messages were then tested to assess their effectiveness. Mothers were receptive to most messages. Minor revisions were made to some messages to improve clarity and increase acceptability. Messages that received strong negative responses were deemed inappropriate for this population. Nutrition professionals working with Asian Indians could use the final messages to inform mothers about developing healthy eating habits in their children.Funded by: MSU AgBioResearch and USDA Multistate Project W1005Grant Funding Source: MSU AgBioResearc and USDA Multistate Project W1005
Anti‐angiogenic Effects of Citrus Polymethoxyflavones and Their Major Metabolites
Authors: Nutakul Wasamon , Zheng Jinkai , Shao Rong , Xiao Hang 
Published: June 2021

Previous studies have demonstrated inhibitory effects of citrus polymethoxyflavones, nobiletin (NBT) and 5‐hydroxy nobiletin (5HN) on several types of cancer. We have identified major metabolites of NBT (i.e. M1: 3′‐hydroxy NBT; M2: 4&#61602;‐hydroxy NBT; and M3: 3′,4′‐dihydroxy NBT) and 5HN (i.e. M4: 3′,5‐dihydroxy NBT; M5: 4′,5‐dihydroxy NBT; and M6: 3′,4′,5‐ trihydroxy NBT) in rodents fed with NBT and 5HN. In this study, we investigated the anti‐angiogenic activities of NBT, 5HN and their major metabolites using wound healing and tube formation assay with Human microvascular endothelial cells. Among NBT metabolites, M2 showed strongest inhibitory effects, while among 5HN metabolites, M4 had the most potent effects. In wound healing assay, M2, M1, NBT and M3 at 50 μM inhibits 50%, 40%, 30% and 10% of cell migration, respectively. M6, M5 and 5HN at 10 μM inhibited 50%, 40% and 30% of cell migration, respectively. Moreover, M4 at only 3μM inhibited more than 90% of cell migration. In tube formation assay, M3 and NBT at 50 μM inhibited 75% and 30% of capillary tubes formed, respectively, while M1 did not inhibit tube formation. M6, M5 and 5HN at 10 μM inhibited 90%, 77%, 54% of tube formation, respectively. Most interestingly, M2 at 50 μM and M4 at 3μM abolished all tube formation. Our results suggested that the number and position of hydroxyl groups in NBT, 5HN and their metabolites dictate their inhibitory effects on angiogenesis.Grant Funding Source : NIH: CA139174, AICR: 10A044
In hypertension CYP450A metabolite 20‐HETE exacerbates flow‐induced arteriolar constriction and promotes cerebrovascular inflammation
Authors: Toth Peter , Csiszar Anna , Sosnowska Danuta , Sonntag William E. , Ungvari Zoltan , Koller Akos 
Published: June 2021

Hypertension impairs local regulation of cerebral blood flow by increasing vascular tone and inducing cerebrovascular inflammation thereby contributing to the pathogenesis of ischemic cerebrovascular diseases (i.e. stroke, vascular cognitive impairment). To test the hypothesis that 20‐hydroxyeicosatetraenic acid (20‐HETE) contributes to hypertension‐induced cerebrovascular alterations, we treated spontaneously hypertensive rats (SHR) with HET0016, an inhibitor of 20‐HETE synthesis. Although HET0016 decreased systolic blood pressure, the treated animals remained hypertensive. In cerebral arteries isolated from HET0016‐treated SHRs flow‐induced constriction was attenuated and endothelial dilation to acetylcholine was improved. HET0016 treatment inhibited cerebrovascular inflammation in SHRs as shown by the reduced expression of pro‐inflammatory cytokines TNF&#61537;, IL‐1&#61538; and IL‐6. Taken together, in hypertension increased production of 20‐HETE contributes to cerebromicrovascular inflammation and dysfunction, which likely promote the pathogenesis of ischemic cerebrovascular diseases.Supported: AHA, Founders Aff., 0855910D, NIH PO‐1 HL‐43023, Hungarian Natl. Sci. Res. Fund (OTKA‐K71591, K67984), MHT 2011.
Exercise training and muscle microvascular oxygenation: role of nitric oxide bioavailability
Authors: Hirai Daniel M , Copp Steven W , Ferguson Scott K , Holdsworth Clark T , Musch Timothy I , Poole David C 
Published: June 2021

Exercise training induces multiple adaptations within skeletal muscle that may improve local O2 delivery‐utilization matching (i.e., microvascular O2 pressure; PO2mv). We tested the hypothesis that increased nitric oxide (NO) bioavailability partly underlies improved muscle PO2mv kinetics from rest to contractions after exercise training. Rats were assigned to sedentary (S; n=18) or treadmill exercise trained (ET; n=10; 60 min/d, 5 d/wk, ~8 wks, 35 m/min; ‐14% grade) groups. PO2mv was measured via phosphorescence quenching in the spinotrapezius muscle at rest and during 1 Hz twitch contractions under control (CON, Krebs‐ Henseleit), SNP (NO donor; 300 μM) and L‐NAME (NO synthase blockade; 1.5 mM) superfusion. ET rats had greater VO2peak than S rats (S: 72 ± 2; ET: 81 ± 1 ml/kg/min; p<0.05). The rate of PO2mv fall during contractions was defined as ΔPO2mv/τ (where τ = time constant) and expressed in mmHg/s. Exercise training slowed ΔPO2mv/τ during CON (S: 1.46 ± 0.14; ET: 0.96 ± 0.14; p<0.05). Compared to CON, SNP slowed ΔPO2mv/τ only in S rats (S: 0.34 ± 0.06; ET: 0.65 ± 0.17; p<0.05) whereas L‐NAME speeded ΔPO2mv/τ only in ET rats (S: −12%; ET: 34%; p<0.05). Exercise training leads to greater microvascular oxygenation at the onset of contractions partly via increased NO bioavailability which likely constitutes an important mechanism for training‐induced metabolic adaptations.(AHA Midwest Affiliate, NIH HL‐108328)
MMP2 deficient mice are protected from hydronephrosis after unilateral urethral obstruction
Authors: Tveitarås Maria Kathrine , Skogstrand Trude , Helle Frank , Leh Sabine , Reed Rolf K , Chatziantoniou Christos , Hultström Michael 
Published: June 2021

Matrix Metalloprotease 2 (Mmp2) is a collagenase known to be important in the development of renal fibrosis. In unilateral urethral obstruction the obstructed kidney (UUO) quickly develops fibrosis, while the contralateral (CL) does not. The fibrotic process in Mmp2 deficient mice (KO) was investigated using heterozygote (HZ) and wild‐type mice as controls (WT).UUO caused hydronephrosis, dilation of renal tubules, loss of parenchymal thickness, and fibrosis after one week. Sirius red quantification of fibrous collagen showed 0.13±0.03% positivity in CL and 0.33±0.05% in UUO (p<0.05). KO‐UUO developed less severe hydronephrosis and had preserved renal parenchyma.Out of 48 genes quantified by PCR 26 were differentially expressed by ANOVA (p<0.05). 25 genes were up‐regulated in UUO wild‐type mice: Adamts1, ‐2, Col1a1, ‐2, ‐3a1, ‐4a1, ‐5a1, ‐ 5a2, Dcn, Fbln1, ‐5, Fmod, Fn1, Itga2, Loxl1, Mgp, Mmp2, ‐3, Nid1, Pdgfb, Spp1, Tgfb1, Timp2, Trf, Vim. Only 18 genes were differentially expression in KO‐UUO. Mmp9 was up regulated, while Mmp2, Fn1, Loxl1, Col5a1, Fbln5, Fmod, Fbln1 and Col5a2 were not changed in KO‐UUO.In conclusion, Mmp2 KO protects against hydronephrosis after UUO and shows milder changes in gene expression compared to WT.The study was supported by the Western Health Authority of Norway, Magn. Bergvall foundation and Lars Hiertas Minne Foundation.
CFTR Dependent Bicarbonate Secretion in Native Small Airway Epithelia
Authors: Shamsuddin A K M , Quinton Paul M 
Published: June 2021

Loss of bicarbonate (HCO3−) transport may play a major role in pathological changes in airways, especially in Cystic Fibrosis (CF). In the small intestine normal mucus release requires CFTR dependent HCO3− secretion. HCO3− may also be crucial for effective bactericidal activities of antibiotics as well as innate antimicrobials. Evidence indicates that HCO3− secretion is present in normal, but defective in CF cultured airway cells. However, whether HCO3− is secreted in native small airways is not known. We have developed a mini‐Ussing system and assayed HCO3− transport in native small airways of pigs and humans indirectly as the changes of transepithelial potential and equivalent short circuit current. With bilateral 25 mM NaHCO3− plus 125 mM NaGlu Ringers’ with amiloride in the lumen, we stimulated with different cAMP and Ca2+ mediated agonists and inhibited with known blockers of HCO3− transport. Results showed that the native small airway epithelia are capable of secreting CFTR dependent HCO3−. HCO3− secretion is physiologically regulated, and probably critical to normal innate defense mechanism of the airways. Failure to secrete HCO3− may cause poor mucociliary and pathogen clearance and may be a target for therapy.Supported by the Nancy Olmsted Trust, NIH (R01‐HL084042) and Cystic Fibrosis Foundation.
Metformin severely impairs in vivo muscle oxidative capacity in a rat model of type 2 diabetes
Authors: Prompers Jeanine J , Wessels Bart , Ciapaite Jolita , Nicolay Klaas 
Published: June 2021

ObjectiveTo investigate the effects of metformin on in vivo and in vitro skeletal muscle mitochondrial function in Zucker diabetic fatty (ZDF) rats using 31P magnetic resonance spectroscopy (MRS) and high‐resolution respirometry (HRR), respectively.Methods12‐week old healthy (fa/+) and diabetic (fa/fa) ZDF rats were treated with metformin (0, 30, 100 or 300 mg/kg body weight/day) for 15 days by oral gavage. At day 14, in vivo 31P MRS was performed on the tibialis anterior (TA) muscle to measure PCr recovery. At day 15, animals were killed and TA muscles were excised for in vitro HRR measurements.ResultsMetformin treatment decreased PCr recovery rates in a dose‐dependent manner in both healthy fa/+ and diabetic fa/fa rats. Whereas, the clinical dose of 30 mg/kg/day had no significant effect, PCr recovery rates were ~22% and ~47% decreased at 100 and 300 mg/kg/day. HRR measurements showed a similar, but less pronounced effect of metformin on in vitro mitochondrial function.ConclusionMetformin treatment impairs in vivo skeletal muscle oxidative capacity in rats in a dose‐dependent manner. This research was funded by a VIDI grant from the Netherlands Organisation for Scientific Research (NWO).
Downregulation of AT1 receptor in the RVLM induced by mesenchymal stem cells treatment prevent the hypertension and sympathetic hyperactivity in 2K‐1C Wistar rats
Authors: Oliveira-Sales Elizabeth Barbosa , Maquigussa Edgar , Semedo Patricia , Oliveira Luciana G. , Câmara Niels O.S. , Bergamaschi Cassia T. , Boim Mirian A , Campos Ruy R 
Published: June 2021

Current approaches to pharmacological treatment of renovascular hypertension are problematic and thus, alternative therapies are needed. We investigated the effects of mesenchymal stem cells (MSC) treatment on systolic arterial pressure (SAP), renal sympathetic nervous activity (rSNA) and AT1 receptor (AT1R) expression in the rostral ventrolateral medulla (RVLM) in an experimental model of renovascular hypertension, 2 Kidney‐1 clip (2K‐1C). Fluorescently tagged MSC (2×105cells/animal, IV) were injected weekly after the 3rd week of renal artery occlusion and the experiments were performed at the end of 6 weeks after clipping. The rats were divided in control group (n=5), control group treated with MSC (n=2), 2K‐1C (n=8) and 2K‐1C treated (n=7). Bilateral punches were taken from the RVLM to perform AT1R protein expression analyses by western blotting. Tracking assays by citometry showed MSC in the medulla oblongata. SAP in 2K‐1C‐treated rats was lower compared to untreated animals (2K‐1C, 224 ± 8 vs 173 ± 6 mmHg, p<0,05) at 6th week followed by a significant decrease in rSNA (27%). MSC treatment reduced brainstem AT1R expression only 2K‐1C rats (28%, p<0,05). Therefore, the results suggest MCS treatment can both prevent the increase in SAP as well as reduce the sympathetic hyperactivity and the expression of AT1R in the RVLM, constituting a future alternative for the treatment of this type of hypertension.Supported by CAPES
VEGF up‐regulation and vascular area enlargement induced by intermittent hypoxia in the rat carotid body is not secondary to oxidative stress
Authors: Iturriaga Rodrigo , Moya Esteban A , Rio Rodrigo Del 
Published: June 2021

Chronic intermittent hypoxia (CIH), a main feature of obstructive sleep apnea, potentiated the carotid body (CB) chemosensory responses to acute hypoxia, enlarges the vascular area and increased the VEGF expression in the CB. Since oxidative stress plays an essential role in the CIH‐induced CB chemosensory potentiation and by the fact that VEGF may be directly up‐regulated by oxidative stress, we hypothesized if the treatment with an antioxidant may impede the increased expression of VEGF and the enlarged vascular area in the CB of rats exposed to CIH. Thus, we tested the effects of ascorbic acid on the vascular area enlargement and the VEGF immunoreactivity (VEGF‐ir) in the CB of rats exposed to 5%O2, 12 times/hr for 8 hrs or sham condition for 21 days. We found that CIH increased VEGF‐ir and enlarged the vascular area in the CB by increasing the size of the blood vessels, although the number of blood vessels was unchanged. Ascorbic acid, which prevented the CB chemosensory potentiation to hypoxia failed to impede the vascular enlargement and the increased VEGF‐ir in the CB. Thus, our results suggest that CB vascular changes, including VEGF up‐regulation may result of the direct hypoxic stimulation during CIH exposure, and not secondary to the increased oxidative stress, which is involved in the potentiation of the CB chemosensory responses to hypoxia.Supported by FONDECYT 1100405
Electrophysiological analysis of the spinal network function in the in situ adult interferon regulatory factor 8 (IRF8) knockout mice
Authors: Yazawa Itaru , Yoshida Yuko , Yoshimi Ryusuke , O'Donovan Michael , Ozato Keiko 
Published: June 2021

IRF8 is a transcription factor expressed mainly in myeloid cells, such as macrophages and microglia (macrophage‐like cells in the CNS). It provides innate resistance to infectious pathogens. IRF8 also directs the development of myeloid cells. Thus, IRF8−/− mice develop a leukemia‐like disease, where granulocytes (neutrophils) are systemically increased, even in the spinal cord. IRF8−/− macrophages and microglia are defective in functions, including cytokine production.We electrophysiologically investigated whether the alterations arising from the absence of IRF8 influence the spinal network function of the adult IRF8−/− and wild type mice (P11 to 12 wks) with the in situ whole and hindlimb preparation. Neuronal discharge was obtained from the phrenic and bilateral peripheral motor nerve. In both mice, locomotor‐like discharge and episodes were induced by the modulated sympathetic tone and by the drug (serotonin, N‐methyl‐D,L‐aspartate, and noradrenalin). Comparisons of episodes, induced by the modulated sympathetic tone and/or by the drug, demonstrated that the lumbosacral cord of IRF8−/− mice was functionally immature. Our results suggest the possibility that IRF8 plays a role in normal development of the spinal network function, possibly through the regulation of myeloid cells in the CNS.Supported by NINDS and NICHD, National Institutes of Health.
Telomere dysfunction as a tool to identify novel DNA damage factors
Authors: Bartocci Cristina , Yates John , Denchi Eros Lazzerini 
Published: June 2021

The DNA damage response (DDR) pathway plays an essential tumor suppressive role ensuring the integrity of genomic information. Two major limitations have hindered the research in this field: i) the unpredictable location of DNA damage sites induced by conventional DNA damage‐inducing agents, ii) the lack of a technique for the isolation of proteins associated with a given DNA substrate. I have overcome these limitations by taking advantage of: i) telomere dysfunction as a tool to induce DNA damage to specific genomic loci, ii) a novel technique developed to isolate proteins associated with specific chromatin loci termed Proteomics of Isolated Chromatin segments (PICh). I performed the PICh purification on Terf2F/F Rosa26‐Cre‐ERT2 mouse embryonic fibroblasts (MEFs), in which deletion of both alleles of Terf2 gives rise to a DDR at chromosome ends. The purification identified 95 proteins uniquely associated with dysfunctional telomeres, among which I selected a subset of candidates for confirmation of their localization to damaged telomeres and for their characterization as potential novel DDR factors.Research Support Source ADI
The Characterization and Identification of Ceramide‐1‐Phosphate Binding Proteins
Authors: Ward Katherine E , Stahelin Robert V 
Published: June 2021

The activation of cytosolic phospholipase A2 α (cPLA2α) has been implicated in atherosclerosis and cerebral ischemia in previous animal models. The sphingolipid metabolite ceramide‐1‐phosphate (C1P) is known to specifically regulate the activation of cPLA2α and has been shown to increase enzymatic activity 5–10 fold through increased membrane residence. We have recently determined the amino acids that are responsible for C1P binding to cPLA2α in vitro and in a cellular system. In addition to heart disease, the conversation of ceramide to C1P has been implicated in cancer and phagocytosis signaling, suggesting that there are unidentified proteins that are regulated by C1P binding in membranes. Using the novel cPLA2α consensus sequence to search the proteome, we have predicted and are currently investigating new C1P binding proteins. Through the characterization of the C1P binding site, we have constructed a novel model for C1P recognition in membranes that deviates from the traditional lipid binding mechanism. This molecular characterization provides great insight into the molecular basis of C1P recognition and selectivity in biological membranes and will significantly increase the molecular basis of C1P binding by proteins. The understanding of this binding site in particular would lay the groundwork for a promising therapy for heart disease.AHA 11PRE7640028 (KEW)NIH T32GM075762 (KEW)
Expression of constitutively active Jak2 in the hypothalamus leads to weight gain that correlates with increased SOCS3 levels
Authors: Ryder Daniel J , Nabilsi Nancy , Sayeski Peter , Scarpace Philip 
Published: June 2021

The leptin pathway is of great clinical interest for weight loss. However, intricate feedback signals obscure viable strategies to affect leptin‐mediated weight loss. We aim to understand this pathway and determine if a constitutively active positive regulator of leptin signaling, Jak2 V617F, alters weight gain and energy intake.Hypothalamic injection of pLentiV617F and pLenti‐GFP was carried out. Rats were given high fat diet and monitored for food intake/weight changes. Oxygen consumption and fat pad analysis was conducted. After tissue extraction QPCR was used to verify expression of transgenes and evaluate levels of endogenous Jak2 transcript and immunoblot to measure Jak2 and SOCS3 protein.Body weight, intake and food efficiency for the V617F rats was up. Concordantly, respiration and voluntary wheel running activity was down. Transgene expression was elevated, as expected, along with leptin and hypothalamic SOCS3 protein in V617F‐injected rats.V617F is indicated to cause caloric increase and metabolic decrease. SOCS3 was up, indicating induction of an inhibitory pathway. We suspect this obese phenotype is caused by an inhibition of Jak2 signaling by SOCS3 in the hypothalamus. This delicate balance between Jak2 expression and metabolic/energy intake regulation and stands as a cautionary tale for pharmacologists who choose to alter these proteins by pharmacological means.
New IMAC media enabling purification of histidine‐tagged proteins directly from eukaryotic cell culture supernatants
Authors: Granér Therese , Algotsson Mattias , Andersson Lars C , Björner Maria , Carlsson Marianne , Glad Gunnar , Hedlund Helena , Hörnsten Lena , Le Grevès Pierre , Lindgren Helena , Lindqvist Staffan , Öberg Katarina 
Published: June 2021

Immobilized metal affinity chromatography (IMAC) purification of secreted histidine‐tagged proteins in eukaryotic cell culture supernatants is often problematic. Incompatibility with the cell culture media appears as stripping of the immobilized metal ions required for binding of target proteins. Due to low target protein concentration in cell culture supernatants, large sample volumes are often needed, aggravating the stripping effect.In this study, purifications of histidine‐tagged proteins were performed using two novel Sepharose™ based IMAC media; Ni Sepharose excel and magnetic His Mag Sepharose excel. Both media have a new type of chelating ligand with exceptionally strong binding of nickel ions. Data showing successful purification of histidine‐tagged proteins from CHO cell culture supernatants will be presented.Furthermore, the characteristics of new media enabled purification of target protein from insect cell culture supernatants. The purification was easily scaled up from 20 μl His Mag Sepharose excel beads to 1 mL pre‐packed columns.