bluuebunny/crossref_metadata_2025_split huggingface dataset:
Improved Postprandial Glycemia and Appetite Scores after Addition of the Ancient Grain Salba (Salvia Hispanica L.) vs Flax to an OGTT: Possible Effect of Viscosity
Authors: Vuksan Vladimir , Choleva Lauryn , Perrin‐Houdon Solenne , Rogovik Alexander , Fairgrieve Christopher , Jenkins Alexandra 
Published: June 2021

ObjectiveTo compare the effects of Salba and flax, two nutritionally similar, high fiber grains whose main difference is viscosity, on postprandial glycemia and appetite.MethodsUsing an acute randomized, single‐blind, crossover design, 9 healthy subjects (4M:5F; BMI 22.7±4 kg/m2) received, on 3 different occasions, a 50g glucose drink alone or with either 25g Salba or 31g flax added, which were matched for fiber. Capillary blood was taken and hunger questionnaires completed at fasting, 15, 30, 45, 60, 90 and 120 min post‐consumption. Viscosity was measured using a Brookfield Dial Viscometer.ResultsThe viscosity of Salba was approximately 3 times higher than that of flax. Salba significantly reduced the glucose iAUC compared to control (p=0.049), whereas flax did not. Salba and flax consumption increased 2hr satiety scores compared to control by 83% and 55%, respectively (NS).ConclusionsAddition of Salba, but not flax, to a glucose drink significantly lowers postprandial glycemia. Although Salba increased satiety to a greater extend than flax, this did not reach statistical significance. These preliminary data suggest that the greater effectiveness of Salba may be due to its higher viscosity level. Further research is warranted to assess the effects of Salba on postprandial glycemia and appetite control.Research support: Salba Smart Natural Products, Denver, CO, USA.
Effect of viscosity and fermentability of purified non‐starch polysaccharides (NSP) on kinetics of net glucose and short chain fatty acids (SCFA) portal flux and insulin secretion in porto‐arterial catheterized pigs
Authors: Hooda Seema , Matte J Jacques , Vasanthan Thavaratnam , Zijlstra Ruurd T 
Published: June 2021

The NSP may lower glycemic and insulin responses, but specific contributions of viscosity and fermentability are unknown. Thus, the effects of NSP on net nutrient portal flux and insulin responses were studied in 4 pigs with 2 catheters [portal vein, carotid artery] and 1 blood flow probe [portal vein]. Semi‐purified [cornstarch, casein] diets supplemented with 5% purified NSP sources were fed in a 2 (low, high viscous; V) × 2 (low, high fermentable; F) factorial arrangement using: low V, low F cellulose (CEL1), high V, low F carboxymethylcellulose (CMC), low V, high F cellulose (CEL2), and high V, high F oat β‐glucan (HVG). Blood was sampled for 12 h postprandially and net nutrient portal flux and insulin secretion were calculated from plasma portal‐arterial differences × flow. Blood flow, portal and carotid glucose and net glucose portal flux peaked at 45 min after feeding (P<0.001) and were not affected by NSP. However, fermentable NSP (CEL2 and HVG) increased (P<0.05) net glucose portal flux 46% over 12 h postprandially. Insulin secretion was 44% lower (P<0.05) for viscous than non viscous NSP. The CEL2 and HVG diets increased (P<0.05) net SCFA portal flux for propionate and butyrate 48%, indicating increased colonic fermentation. In conclusion, viscosity of NSP reduced insulin secretion and fermentable NSP increased net portal flux of glucose, propionate, and butyrate.Grant Funding Source: ALMA, Danisco, and Alberta Pulse Growers
Regulatory Role of Mucosal Maltase‐Glucoamylase in Starch Digestion and Glucose Homeostasis
Authors: Diaz‐Sotomayor Maricela , Avery Stephen E , Chacko Shaji K , Quezada‐Calvillo Roberto , Yan Like , Hamaker Bruce R , Nichols Buford L 
Published: June 2021

Slower rates of starch digestion by sucrase‐isomaltase (Si) in Mgam null mice may fail to regulate gluconeogenesis (GNG). Mgam nulls have 40% reduction of glucose production from starch.AimMeasure glycemic index and rate of gluconeogenesis (fGNG) as fraction of total glucose appearance (Ra) and glucogenesis from starch (MPE) by Mgam null and WT mice.MethodsGroups of 4–8 null or WT mice were on low 13C‐diet and trained to feed from 12–13 h after previous feed (hAF). D2O was given IP at 2 hAF. 13C‐enriched starch was fed from 12–12.5 or 13 hAF and intake weighed. Blood was obtained by tail nicking at 5, 12, 12.5, 13, 14, and 16 hAF and decapitation at 14 or 16 hAF. Blood glucose was by glucometer and spotted on filter paper for MS. Glucose was derivatized as penta‐acetate and run by GC‐C‐IRMS for 13C‐glucose (MPE) and for 2H‐C5‐glucose (fGNG) enrichments by GC‐MS. Body D2O dilution was by IRMS.ResultsInverse correlation between MPE and fGNG was found (R‐Sq 86%). At 14 hAF 0.5, but not 1.0 g, feeds, WT MPE exceeded null (p 0.02). Fasted fGNG averaged 71% and when fed null fell to 30% and WT to 20% (p 0.03). 1 gm intakes increased MPE only of null consistent with known in‐vitro substrate inhibition of Mgam.Summary: Mgam activity regulates fGNG and is critical for starch digestion at snacking (0.5 g) but not at feasting (1 g) intakes. Mgam deficiency was compensated by increased fGNG. Glycemic index was regulated both by MPE and GNG pathways.
Dentin matrix protein 1 induces endothelial cell cycle arrest and differentiation through VE‐cadherin
Authors: BELLAHCENE Akeila , Pirotte Sophie , Mottet Denis , Ormenese Sandra , Castronovo Vincent 
Published: June 2021

Dentin matrix protein 1 (DMP1) is a member of the Small Integrin‐Binding LIgand N‐linked Glycoproteins (SIBLINGs) family, a group of proteins initially described as mineralized extracellular matrices components and more recently implicated in several key steps of cancer progression, including angiogenesis. Although pro‐angiogenic activities have been demonstrated for two SIBLINGs, the role of DMP1 in angiogenesis has not been addressed yet. We found that DMP1 inhibited the proliferation while it stimulated migration and tubulogenesis of human umbilical vein endothelial cells (HUVEC), thus promoting differentiation of endothelial cells. Further investigation of DMP1 mechanism of action evidenced a CD44‐dependent G1‐block and an increased p27Kip1 and VE‐cadherin expression in HUVEC.Our data identify DMP1 as a new regulator of angiogenesis that turns on the switch of the endothelial cell phenotype from proliferative to differentiated, through a CD44‐dependent differentiation program that links up with a VE‐cadherin pathway mediating contact inhibition of endothelial cell growth.
Interstitial flow induces vascular SMC migration in collagen I gels regulated by MMP‐1 via an ERK1/2‐dependent and c‐Jun‐mediated mechanism
Authors: Shi Zhong‐Dong , Tarbell John M 
Published: June 2021

Smooth muscle cells (SMC) migration into the intima after vascular injury is a central process in vascular lesion formation. The transmural interstitial flow is observed after damage to the vascular endothelium. In this study, the direct effects of interstitial flow on SMC migration were investigated in a 3‐dimensional collagen I gel system.Exposure of gels to a differential pressure of 1 cmH2O induced interstitial flow (shear stress ~0.05 dyn/cm2) that substantially enhanced cell migration rate. Gene silencing suggested that flow‐induced migration was controlled by matrix metalloproteinase (MMP)‐1. PD‐98059, an ERK1/2 inhibitor, completely abolished flow‐induced migration and MMP‐1 expression. PD‐98059 also inhibited flow‐induced ERK1/2 activation and c‐Jun and c‐Fos expression. Silencing ERK1/2 or c‐jun completely abolished SMC migration and/or MMP‐1 expression, while knocking down c‐fos did not affect MMP‐1 expression. We also found that p38 MAPK and NF‐κB did not play major roles in flow‐induced MMP‐1 expression and cell migration.Taken together, our data indicate that interstitial flow induces MMP‐1 expression which in turn digests collagen matrix and promotes SMC migration via an ERK1/2‐dependent and c‐Jun‐mediated mechanism and suggest that interstitial flow may play an important role in SMC migration and neointima formation. Supported by NIH NHLBI grant RO1 HL 57093.
Roles of NF‐kB and STAT3 in CXC chemokine‐mediated hepatocyte proliferation and cell death
Authors: Clarke Callisia N , Sakai Nozomo , Tevar Amit D , Edwards Michael J , Lentsch Alex B 
Published: June 2021

BACKGROUNDCXC chemokines have divergent effects on hepatocytes. After hepatic I/R CXC chemokines are expressed at high levels and promote liver injury. After partial hepatectomy, they are expressed at low levels and promote proliferation. Previous studies show that chemokines are proliferative at all doses, hepatoprotective at low concentrations, while cytotoxic at high concentrations. Here we explore the roles of NF‐kB and STAT3 in regulating the effects of CXC chemokines in hepatocytes.METHODSHepatocytes isolated from Balb/c mice were stimulated with media alone, or with MIP‐2 at low (10 ng/ml) or high (10,000 ng/ml) concentrations in the presence or absence of inhibitors of NF‐kB (BAY 11‐7085) or STAT3 (AG490) for 24 hrs. Cell death was determined by release of LDH and cell proliferation by DNA incorporation of BrdU.RESULTSStimulation of hepatocytes with low dose MIP‐2 resulted in decreased cellular injury and increased proliferation. Blockade of NF‐kB resulted in massive hepatocyte cell death. Blockade of STAT3 resulted in abrogation of the protective effects of low‐dose MIP‐2. Blockade of STAT3 resulted in a decrease in hepatocyte proliferation with or without MIP‐2.CONCLUSIONSNF‐kB activation is required for hepatocyte viability in vivo. The hepatoprotective effect of low concentrations of CXC chemokines is STAT3 dependent. STAT3 is required for hepatocyte proliferation in vitro.
Immunodeficient mice ‐ A suitable model for cell transplantation in non‐alcoholic steatohepatisis (NASH)
Authors: Stock Peggy , Pelz Sandra , Ebensing Sabine , Hempel Madlen , Brückner Sandra , Richter Kati , Christ Bruno 
Published: June 2021

NASH is a benign disease and will progress, if untreated, into fibrosis/cirrhosis and potentially into HCC. Human cell therapy approaches for the treatment of NASH have not been addressed yet. The present work aimed at establishing an animal model to evaluate the feasibility of stem cell‐derived hepatocytes.Immunodeficient Pfp/Rag2−/− mice were fed a methionin‐cholin‐deficient diet (MCD diet) up to 5 weeks. Alanine aminotransferase (ALT) and triglycerides were determined in the serum. Histological analyses of liver sections were performed to detect structural abnormalities by HE, the collagen distribution by sirius‐red and fat depositions by sudan III staining. Expression of the acute phase protein SAA, the proinflammatory cytokine TNFα, the marker for activated stellate cells αSMA as well as collagen1 in liver tissue were specified by RT‐PCR.Already 3 weeks after feeding the MCD diet, microsections displayed a deteriorated architecture of the liver tissue, which worsened with continued feeding. By HE‐staining massive steatosis and hepatocellular injury were observed and confirmed by sudan III staining in livers of animals fed the MCD diet as compared to animals fed the control diet. Fibrosis in livers of animals on MCD diet was obvious by collagen staining. The marker of hepatocyte fade ALT was significantly higher (2‐fold) in the serum of mice on MCD diet. Serum triglycerides were significantly lower in MCD diet‐fed animals. RT‐PCR analysis revealed elevated mRNA levels of SAA and TNFα as well as of αSMA and collagen1 in the livers of mice fed the MCD diet.Thus, immunodeficient Pfp/Rag2 mice fed with the MCD diet displayed typical features of NASH, which makes this animal model suitable to evaluate pre‐clinically human cell therapy approaches of liver diseases.
Stretching the Limits: Dyad Pedagogy and Technology Bolster Anatomy Learning.
Authors: Noronha Alinea Serena , Ahsan Lusana , Sherman Lloyd R , Marquez Samuel 
Published: June 2021

Dyad Pedagogy (DP) combined with technology enhances student learning in first‐year Anatomy courses for medical students at SUNY Downstate. Two students working together (dyads) solve and/or explore a problem ‐ maximizing feedback between the two over all other approaches ‐ and thus optimizing learning in the cognitive, affective, and psychomotor domains as defined in Bloom's taxonomies of learning. The dyads create a project that applies the principles of gross anatomy to clinical pathologies in a presentation to be captured on HD video. They define muscles and innervations of a particular region of the body and explain issues associated with injury to these structures. The project integrates all learning modalities: textbook, lectures, gross anatomy labs, and the internet and involves three stages of dyad problem‐solving: 1. they become experts in the anatomy of their region of study; 2. they develop a skit to aid in the communication of the clinical relevance of muscle‐nerve damage; 3. they present the project to the class. The presentation is then video‐taped and posted on the Intranet for their classmates to use during review and study. These dyad‐created anatomy videos augment the learning of gross anatomy principles and are adjudged clear and engaging presentations of muscle action. Their value is evidenced by the impact of this learning method on the entire class as measured in terms of their online use.Grant Funding Source: SUNY Downstate
Utilizing peer, near‐peer, and inter‐professional teaching: A model for integrating embryology into gross anatomy curriculum
Authors: Scoville Elizabeth Ann , Nyauncho Clive P , Kumar Neha , Hassinger James Peyton , Lachman Nirusha , Pawlina Wojciech 
Published: June 2021

As embryology becomes increasingly integrated into other basic science courses, questions arise of what teaching method should be used to effectively utilize curriculum time for this subject. At Mayo Medical School, the human structure block integrates gross anatomy, embryology, and radiology. We present a model that utilizes peer and near‐peer teaching, continuous self‐assessment, and inter‐professional collaboration to maximize embryology curriculum time in this integrated course. Students peer teach embryology topics in presentations, and create a patient education pamphlet on a related congenital disorder. Production advice and critique on these pamphlets is provided by an inter‐professional collaboration with the Mayo Clinic patient education department. Third year teaching assistants guide peer teaching with detailed content guides, by reviewing presentations and pamphlets, and being available for near‐peer tutoring. Students are provided with formative feedback in the form of Audience Response System quizzes to assess their learning progress throughout the course. Student satisfaction and utilization of near‐peer and inter‐professional resources will be assessed at the end of the course.Grant Funding Source: Department of Anatomy
Pro‐survival and pro‐apoptotic factors following axotomy in a murine model of Amyotrophic Lateral Sclerosis.
Authors: Haulcomb Melissa M , Mesnard Nichole A , Politis Christine M , Sanders Virgina M , Jones Kathryn J 
Published: June 2021

The facial nerve axotomy is used to study motoneuron (MN) survival and peripheral nerve regeneration. Using this model in wild‐type (WT) mice we have identified two populations of MN; regenerative MN in the ventromedial (VM) subnucleus and degenerative MN in the ventrolateral (VL) subnucleus. Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease caused by MN cell death. In the SOD1 mouse model of ALS, a recent study demonstrated the development of two MN populations, one compensatory and one degenerative, following disease progression. To further examine these findings we propose to use facial nerve axotomy as a tool to characterize pre‐symptomatic SOD1 MN or neuropil response compared to WT. We hypothesize that the axotomy‐induced facial motoneuron loss in SOD1 relative to WT, is due to a pro‐inflammatory microenvironment resulting in apoptosis. RT‐PCR was conducted using laser microdissected control vs. axotomized facial nuclei and VM vs. VL subnuclei to determine axotomy‐induced mRNA expression changes in pro‐apoptotic genes (FasR, Caspase‐3, TNFR1) and pro‐survival genes (PAC1‐R, TNFR2, CX3CR1). Localization of TNFR1, TNFR2, and CX3CR1 will also be examined via immunohistoochemistry.Grant Funding Source: NIH grant NS40433
The role of orexin and dopamine in sleep alterations from the progressive, neurotoxin‐induced model of parkinsonism
Authors: McDowell Kimberly Anne , Quiroz Cesar , Ferre Sergi , Yarowsky Paul 
Published: June 2021

Parkinson's disease (PD) is classically defined as a motor disorder resulting from decreased dopamine (DA) production in the basal ganglia circuit. To better diagnose PD before the onset of severe motor dysfunction, current attention has focused on the early, non‐motor symptoms. Sleep disorders, such as excessive daytime sleepiness (EDS), are one of the most prominent initial symptoms in PD. Recent studies revealed that orexin (ORX) neurons, a cell type vital to sleep regulation, also degenerate in PD and may contribute to the sleep disorders. We have developed a novel, progressive rat model that can investigate this aspect of PD. Epidemiological studies found a link between the Guamanian variant of Amyotrophic Lateral Sclerosis/Parkinsonism Dementia Complex (ALS/PDC) and the consumption of flour made from the washed seeds of the plant, Cycas micronesica (cycad). Cycad‐fed rats displayed a parkinsonian phenotype. Uniquely, these rats also displayed a hypersomnolent behavior similar to EDS and a significant loss of ORX neurons. We hypothesize that the sleep disturbance is due to orexin dysfunction, which then induces a loss of DA neurons in the SN. To measure this altered neurochemistry, we utilized microdialysis and high performance liquid chromatography to determine levels of DA in the SN and caudate putamen of the cycad‐fed rat.Support: NIEHS (KM); NIDA (SF); VA (PY)Grant Funding Source: NIEHS
Environmental Factors Contributing to the Regulation of Insulin Sensitivity in Type 2 Diabetic Patients
Authors: Zierath Juleen Rae 
Published: June 2021

Epigenetic modification through DNA methylation is implicated in metabolic disease and may play a role in the mechanism by which environmental factors influence metabolic responses in diabetes. Using whole genome promoter methylation analysis of skeletal muscle from normal glucose tolerant and Type 2 diabetic subjects, we identified cytosine hypermethylation of Peroxisome Proliferator‐Activated Receptor γ Coactivator‐1 α (PGC‐1α) in diabetic subjects. Methylation levels were negatively correlated with PGC‐1α mRNA and mitochondrial DNA (mtDNA). Bisulfite sequencing revealed that the highest proportion of cytosine methylation within PGC‐1α was found within non‐CpG nucleotides. Non‐CpG methylation was acutely increased in human myotubes by exposure to tumor necrosis factor‐α (TNF‐α) or free fatty acids, but not insulin or glucose. Selective silencing of the DNA methyltransferase 3B (DNMT3B), but not DNMT1 or DNMT3A, prevented palmitate‐induced non‐CpG methylation of PGC‐1α and decreased mtDNA and PGC‐1α mRNA. We provide evidence for PGC‐1α hypermethylation, concomitant with reduced mitochondrial content in Type 2 diabetic patients, and link DNMT3B to the acute fatty‐acid induced non‐CpG methylation of PGC‐1α promoter.Study supported by the European Research Council and the Swedish Research Council.
Drug Resistance in Tuberculosis
Authors: Blanchard John Sears 
Published: June 2021

Drug resistance is a common problem in all bacterial infections, but in the particular case of human Tuberculosis (TB), there are few effective drugs that have been developed and approved for use against the disease. Modern chemotherapy against TB consists of treatment for two months with four drugs (isoniazid, rifampicin, pyrazinamide and ethambutol) followed by an additional four months with isoniazid and rifampicin. Significant resistance to isoniazid began to appear in the early 1980's, while the emergence of strains resistant to both isoniazid and rifampicin began to emerge in the 1990's. These are the two compounds that exhibit bactericidal activity against rapidly growing organisms, and strains exhibiting this resistance pattern are termed multi‐drug resistant (MDR). More recently, strains that are extremely‐drug resistant have been reported around the globe. These strains are resistant to both isoniazid and rifampicin, as well as fluoroquinolones and at least one aminoglycoside. These XDR‐TB strains are extremely difficult to treat effectively, and mortality rates are extremely high for persons infected with XDR‐TB.A large effort is currently underway to identify new lead compounds with novel targets and mechanisms of action. Several candidates in clinical trails will be discussed. In addition, a reexamination of drugs previously not used to treat TB is underway. The mechanisms of action of, and mechanisms of resistance to, both old and newly developing drugs will be discussed.
Native levels and determinants for oxidation of coenzyme Q10 in human plasma
Authors: Franke Adrian A , Morrison Cynthia M , Bakke Jesse L , Custer Laurie J , Li Xingnan , Cooney Robert V 
Published: June 2021

Coenzyme Q10 (Q10) is present in the circulation mainly reduced (ubiquinol‐10; UL10), but oxidizes quickly ex vivo to ubiquinone‐10 (UN10). Therefore, native UL10/UN10 ratios, used as markers of redox status and disease risk, are difficult to measure.We established a RP‐(U)HPLC method with coulometric detection to measure natively circulating UL10 and UN10 concentrations by adding a ubiquinol/ubiquinone mixture as internal standards immediately after plasma preparation. This allowed adjustment for unavoidable artificial UL10 oxidation as well as for total losses (or gains) of analytes during sample storage, processing, and analysis since the internal standards exactly paralleled the chemical behavior of Q10. This technique applied to blood collected from 13 healthy volunteers revealed Q10 levels of 680–3300 nM with a UL10/UN10 ratio of 95:5 (mean) which was inversely associated with total Q10 (r=−0.69; p=0.004).The oxidation of UL10 to UN10 was equimolar, increased by O2, and decreased by lower temperatures or various degassing methods. Although UL10 was stable in blood or when pure in organic solvents at 22 oC, its oxidation was catalyzed dose dependently by alpha‐tocopherol and butylated hydroxy toluene, particularly when present in combination. Key structural features for the catalytic pro‐oxidant properties of phenolic antioxidants included two aliphatic substituents vicinal to the phenolic hydroxyl group.
Family‐Focused Program Shows Benefit in Treating Excess Weight in Children
Authors: Rost Stephanie Lyn , Miller‐Kovach Karen , Angelopoulos Ted , Rippe James M. 
Published: June 2021

OBJECTIVETo assess a parent‐based, pilot program for treating excess weight in children in a community setting.METHODSParents attended 8‐to‐10 weekly sessions led by a coach trained in childhood and adolescent weight issues and supported by local pediatricians in the Tampa and Orlando areas of Florida. Effective parenting techniques to enact evidence‐based, healthy weight recommendations for the entire family were taught and reinforced in an environment of group support. Discussions and written materials focused on behavior and lifestyle change. To determine impact, independent researchers made home visits to measure height and weight of all children in the household at baseline, 8 weeks and quarterly for one year.RESULTS114 children have 59 week results (i.e., at baseline and again 1 year after completion of the 2‐month pilot program). 12 children had a BMI‐for‐Age <85th %‐tile at baseline. Of the 102 children at baseline with a BMI‐for‐Age ≥85th %‐tile, the mean age was 10.3 ± 2.6 years; at baseline, the mean BMI z‐score was 2.01 ± 0.41 and 1.89 ± 0.48 at 59 weeks (p<0.001). 68 children with excess weight reduced their BMI z‐score, 1 stayed the same and 33 increased. The mean BMI z‐score change was +0.14 for those that gained and −0.24 for those that lost.CONCLUSIONA parent‐focused program appears to have a positive influence on children's weight one year after the intervention.Weight Watchers International, Inc.