bluuebunny/crossref_metadata_2025_split huggingface dataset:
Prebiotics and β‐Glucan Affect Jejunal and Serum Alkaline Phosphatase Affinity in Weanling Pigs
Authors: Hayhoe Mychal‐Ann N , Archbold Tania , Fan Ming Z 
Published: November 2023

Biological mechanisms of dietary supplementation of prebiotics and β‐glucan in modulation of health status need further clarification. Given the recognized role of alkaline phosphatases (AP) in detoxification of endotoxin lipopolysaccharides (LPS), we hypothesized that dietary supplementation of three prebiotics and β‐glucan in modulation of health status was mediated through affecting alkaline phosphatase functionality such as maximal enzyme activity (Vmax) and enzyme affinity (Km). This study was conducted to determine effects of dietary supplementation of three prebiotics and β‐glucan at 0.75% instead of feed antibiotics on growth performance, blood urea concentration, fecal scores, jejunal and serum AP kinetics and large intestinal fermentation in weanling piglets fed corn and soybean meal (SBM)‐based diets. Six experimental diets were formulated with corn, SBM and fishmeal as the bulk ingredients. This includes Diet 1, a negative control (NC) of the basal diet with no supplemental feed antibiotics and no tested supplements; Diet 2, a positive control (PC) of the basal diet with supplemental feed antibiotics but no other tested supplements; Diet 3, a retrograded resistant corn starch supplementation of the basal diet with no supplemental feed antibiotics; Diet 4, an oat β‐glucan supplementation of the basal diet with no supplemental feed antibiotics; Diet 5, a Fibersol‐2 supplementation of the basal diet with no supplemental feed antibiotics; and Diet 6, an inulin supplementation of the basal diet with no supplemental feed antibiotics. A total of 216 piglets, 21 d old, with an initial body weight of 7.0 kg, were fed 1 of the 6 diets for 21 d in three study blocks according to a completely randomized block design. Dietary supplementation of the three prebiotics and β‐glucan did not significantly affect growth performance and main intestinal fermentation endpoints. Dietary supplementation of β‐glucan in Diet 4 increased (P<0.05) the wk 1–3 overall fecal score compared with the NC diet. Fibersol‐2 in Diet 5 and inulin in Diet 6 reduced (P<0.05) the Vmax of the proximal jejunal AP compared with the NC diet. The Vmax of serum AP was different (P<0.05) between the β‐glucan Diet 4 and the PC diet. Dietary supplementation of Fibersol‐2 in Diet 5 and β‐glucan in Diet 4 increased the AP affinity by about 1 fold compared with the NC diet. Serum AP affinity Km values were at least 10‐fold higher than the Km values of the jejunal AP, suggesting that the proximal jejunal AP is potentially much more efficient than the serum AP in detoxification of endotoxin LPS. Dietary supplementation of the three prebiotics and oat β‐glucan at 0.75% had little effects on growth performance but might affect the gut and whole body health status via influencing the AP detoxification kinetics in the weanling pig.Support or Funding InformationSupported by the NSERC Discovery and the OMAFRA‐University Partnership Programs.
Intrauterine Nutrient Restriction Programs Impaired Endothelial Function Associated With Functional Dysfunction in Circulating Endothelial Progenitor Cells
Authors: de Oliveira Vanessa Aparecida , Silva Sebastião Donato , de Souza Livia Victorino , Fernandes Tiago , Akamine Eliana Hiromi , de Carvalho Maria Helena Catelli , de Oliveira Edilamar Menezes , Michelini Lisete Compagno , do Carmo Pinho Franco Maria 
Published: November 2023

ObjectiveThis investigation aimed to evaluate the effects of intrauterine nutrient restriction in both, vascular reactivity and functional capacity of endothelial progenitor cells (EPCs) in adult male offspring.MethodsThe procedures bellow were approved by Ethics Committee of Federal University of São Paulo (836880). Pregnant Wistar Rats received to Ad libitum or 50% of Ad libitum diet throughout gestation. At birth, pups were weighted. Adult male offspring from both groups (20 weeks of age) were submitted to femoral artery cannulation to register arterial blood pressure and heart rate. Vascular reactivity were performed by concentration‐response curves to Acetylcholine (ACh: 10−9M‐3×10−5M) and to Sodium Nitroprusside (SNP: 10−9M‐10−6M) in thoracic aorta rings. In addition, protein expression of eNOS phosphorylated in serine1177 by western blotting, and Nitric oxide concentration by NO Analyzer were investigated in thoracic aorta. Circulating EPCs number were characterized as CD34+VEGFR2+ cells in flow cytometer. The functional capacity of circulating EPCs was assessed in vitro by the colony‐forming unit assays. Results are show as mean ± EPM, test t de student were used.ResultsBody weight at birth (Control: 7.01±0.34g vs. Restricted: 4.3±0.08g), confirmed that Intrauterine nutrient restriction leads to intrauterine growth restriction. Intrauterine nutrient restriction did not programed alterations neither in mean arterial blood pressure (Control: 118±3mmHg vs. Restricted: 109±2mmHg), nor in heart rate (Control: 355±13 bpm vs. Restricted: 343±4 bpm). Restricted group exhibited reduction in maximal vascular response to ACh (Control: 92.18±2.7% vs. Restricted: 65.04±4.4%), but normal NPS‐induced vasodilation (Control: 98.45±2.38% vs Restricted: 93.97±2.64%) in aorta rings. Thoracic aorta from restricted offspring showed similar levels in protein expression of eNOS phosphorylated compared to control group (Control: 1.16±0.05 vs. Restricted: 1.05±0.01), on the order hand a reduction in NO concentration were observed (Control: 426.2±63.03μM/mg vs Restricted: 217.8±18.22 μM/mg). In addition, we found that circulating EPCs number was not altered by intrauterine nutrient restriction (Control: 0.008±0.0019 % vs. Restricted: 0.007± 0.0009%), but the number of colony‐forming unit was reduced (Control: 7.75±0.97 vs. Restricted: 3.80±0.82).ConclusionOur data suggests that intrauterine nutrient restriction programs endothelial dysfunction in adult offspring, which can be associated in part with reduction in NO concentration and impairment in EPCs functional capacity.Support or Funding InformationFAPESP
Prevalence of Staphylococcal Diarrhea in some Developing African Countries
Authors: Einstein George P , Tulp Orien L , Oyesile T C , Obidi O F 
Published: November 2023

BackgroundStaphylococcal diarrhea is a common gastro intestinal illness caused majorly by poor water supply and unhygienic food preparation. Although, about 70% of diarrheal cases per year have been attributed to the consumption of contaminated foods, in Africa, few studies have reported the incidence of Staphylococcus‐related diarrhea and the implicated virulence factors.ObjectivesTo investigate the implications of common factors such as enterotoxin production, enzyme production, inadequate sanitary conditions, type of food and use of antibiotics on the burden of staphylococcal diarrhea.MethodsA literature search was performed using Pubmed, Googlescholar, American society for microbiology (ASM) journals and other sources. The quality of studies was assessed. Adjusted odds ratios with 95% confidence intervals (CI) for the occurrence of staphylococcus aureus amongst other causes were extracted. For each study, a multivariate logistic regression analysis of the adjusted odds ratio was performed to identify the risk factors on the burden of staphylococcal diarrhea.FindingsSeven case‐control studies were included in the meta–analysis. Quality of individual studies rages from 0.57–0.84 (median, 0.69). Meta‐analysis based on burden of staphylococcal diarrhea gave pooled odds ratios 3.27 (95% CI; 2.88–4.17). The results identified inadequate sanitary conditions and type of foods as the risk factors for the burden of staphylococcal diarrhea in Africa.ConclusionImproved personal and environmental hygiene should be intensified through health education to enhance good living conditions.Support or Funding InformationSupported by Institutional Resources of USAT, the Einstein Institute and the University of Lagos
Effect of Vitamin D Fortified Cheese on Oral Glucose Tolerance in Individuals Exhibiting Marginal Vitamin D Status and an Increased Risk for Developing Type 2 Diabetes: A Double‐Blind, Randomized Placebo‐Controlled Clinical Trial
Authors: Moreira‐Lucas Tracy S , Duncan Alison M , Rabasa‐Lhoret Remi , Vieth Reinhold , Gibbs Alison , Badawi Alaa , Wolever Thomas MS 
Published: November 2023

Epidemiological data suggest that vitamin D may play a role in glucose metabolism and homeostasis, and that it maybe particularly important for individuals at an increased risk for developing type 2 diabetes mellitus (T2DM).ObjectiveWe conducted a double‐blind, randomized, placebo‐controlled trial to examine the effects of 28,000 IU of vitamin D3 given in cheese once per week versus placebo on the 2hr oral glucose tolerance test (OGTT) and measures of insulin sensitivity, secretion and β‐cell function.Study DesignPotential participants were identified as being at an increased risk for developing diabetes using the Finnish Diabetes Risk Score (FINDRISC) questionnaire. Participants who were vitamin D deficient (serum 25‐hydroxy vitamin‐D [25(OH)D] ≤65nmol/L) and who had elevated glycated hemoglobin (HbA1c) between 5.4 and 6.4% and/or fasting glucose between 5.6 and 6.9 mmol/L were randomized to receive 28,000 IU of vitamin D3 or placebo (20 IU) once weekly for a period of 24 weeks. The primary outcome of interest was the difference in plasma glucose 2hr after an OGTT between baseline and 24 wks. Secondary outcomes include fasting glucose, fasting and postprandial insulin and indices of insulin sensitivity (Matsuda Index), secretion (insulinogenic index), β–cell function (ISSI‐2) and long‐term glycemic status (HbA1c). Data were analyzed by intention‐to‐treat.ResultsSeventy‐one participants (mean age 47.4) were randomized and sixty‐three completed the trial. Supplementation produced a significant increase in serum 25(OH)D in the vitamin D group (n= 35) versus placebo (n=36) (103.6±36.5 vs. 46.4±18.9 nmol/ L, p <0.0001). After 24 wks of supplementation 74% of participants in the vitamin D group achieved 25(OH)D levels ≥75nmol/Lvs6% in the placebo group. Supplementation produced no significant improvements in fasting (p=0.89) and glucose 2hr after the OGTT (p= 0.88), fasting (p= 0.28) and postprandial (p= 0.77) insulin, HbA1c (p=0.34), HOMA‐IR (p= 0.32), Matsuda Index (p=0.72), and ISS1‐2 (p=0.86).ConclusionWeekly doses of 28,0000 IU of vitamin D3 for 24 wks in a group of multi‐ethnic, vitaminD–deficient individuals identified as being at high risk for developing T2DMdid not improve oral glucose tolerance, insulinsensitivity, β–cell function or HbA1c.Support or Funding InformationResearch funded by the Dairy Farmers of Canada and the Public Health Agency of Canada.
Evaluating the Effect of Seizure Induction on Top of HFCD and/or Vitamin E Administration on the Levels of Oxidative Stress Biomarkers in the Hippocampus
Authors: Hasan Zuheir A , Alzoubi Karem H 
Published: November 2023

There is increasing evidence that oxidative stress is a casual factor in different neurodegenerative disorders such as Alzheimer disease and epilepsy. We have previously shown that consumption of High‐fat high‐carbohydrate diet (HFCD) induces oxidative stress, which results in hippocampal neuronal damage hence impairment of learning and memory, which was reversed by the antioxidant Vitamin E. The reported damage in the hippocampus caused by oxidative stress following consumption of HFCD could alter synaptic transmission in the hippocampus and may increase susceptibility to seizures. Recently, we showed that chronic consumption of HFCD increases, whereas Vitamin E decreases susceptibility to chemically induced seizures using the PTZ seizure threshold model in rats. The present study was undertaken to determine the effect of seizure induction on top of HFCD and/or Vitamin E consumption on the levels of oxidative stress biomarkers in the hippocampus. Male Wistar rats (250–300 gms) were randomly assigned into four groups: control, high‐fat high‐carbohydrate diet (HFCD), vitamin E (Vit E), and high‐fat high‐carbohydrate diet with vitamin E (HFCD + Vit E). Vitamin E and/or HFCD were concurrently administered to animals for 6 weeks. Thereafter, PTZ seizures were induced in half of the animals from each group, whereas the rest of the animals were kept as a control without seizure induction. Thirty minutes later, all animals were killed and hippocampus tissues were extracted for molecular analysis of oxidative stress biomarkers (GSH, GSSG, GSH/GSSG ratio, GPx, SOD, and catalase) using ELISA technique. Results revealed that PTZ seizures were associated with significant increases in oxidative stress biomarkers. These increases were amplified in rats consuming HFCD, whereas they were reduced in rats concurrently administered vitamin E. In rats chronically consuming HFCD and concurrently treated with vitamin E, PTZ seizures induced changes in oxidative stress biomarkers were similar to that in control animals. These data suggest that during the course of PTZ‐induced seizure, prolonged consumption of HFCD increases susceptibility to oxidative stress in the hippocampus. Such an effect is being normalized by concurrent administration of vitamin E.Support or Funding InformationSupported by Grants from Jordan University of Science and Technology and Arabian Gulf University
Zinc supplementation activates Nfe2l2/ARE‐MT2‐antioxidant pathway in a model of diabetic nephropathy
Authors: Ding gangqiang , Hao Mary , Tian Peiyao , Tang Qingping , Zhao Hong , Darzynkiewicz Zbigniew , Ferreri Nicholas R. , Hao Shoujin 
Published: November 2023

We previously showed that metallothioneins (MTs) can be induced by zinc supplementation. The contribution of this mechanism to the regulation of MTs was determined both in vitro and in vivo by the activating Nfe2l2/ARE antioxidant pathway with zinc supplementation in this study. Diabetic male mice (age: 12 wk) were induced using streptozotocin (STZ), then divided into 2 groups and treated with zinc or vehicle. Liver and kidney Zn were increased after dietary Zn for 3 weeks; no significant increase in plasma zinc concentration. Systemic and intrarenal oxidative stress was reduced by zinc supplementation by examination of 8‐hydroxyde‐oxyguanosine (8‐OHdG) in the kidney tissues and urine. The expression of nuclear factor erythroid 2‐related factor 2(Nfe2l2) significantly increased for kidney tissues in the zinc‐treated group compared to the vehicle‐treated group. In contrast, protein expression of nuclear factor‐kB p65 in the kidney decreased in the zinc‐treated group compared to the vehicle‐treated group. Interestingly, MT2 gene expression in renal cortical tubules was also found to increase approximately 54% in the zinc‐treated group compared to the vehicle‐treated group, despite no significant increase for other MT isoforms. Pretreatment of primary renal tubular epithelial cells with an activator digitoflavone of Nfe2l2 before H2O2 exposure significantly decreased oxidant generation and cytotoxicity, whereas Nfe2l2 inhibition and gene silencing (shRNA) exacerbated the injury in vitro studies. Anti‐genotoxic effect of MTs was evident in prevention of DNA damage and micronucleus formation after in renal tubular epithelial cells pretreated by adding MTs (mixture of MT1 and MT2). The MT2 gene silencing in renal tubular epithelial cells significantly increased reactive oxygen species generation and provided marked protection against H2O2‐induced cytotoxicity. Thus, the present study shows that Zinc supplementation attenuates oxidative stress via Nfe2l2/ARE‐MT2 pathway in a model of diabetic nephropathy.Support or Funding Information973 project, National Natural Science Fund Project, NIH
Comparison of Macro Mineral Contents following Kind of Vegetables produced in Korea
Authors: Hwang Jin Bong , Park Eun‐Joo , Kim Soyoung , Seo Dongwon , Choi Youngmin , Kim Se‐Na , Nam Jin‐Sik , Yang Mi‐Ok 
Published: November 2023

Recently, macro minerals (Na, Ca, K Mg and P) have the excellent functions associated with prevention of disease. We estimated an amount of macro minerals in the vegetables produced in Korea in order to build the food nutritional ingredient table. A SRM 1849a purchased from NIST in USA was digested by the microwave and validation of macro minerals in SRM 1849a was carried out by inductively coupled plasma optical emission spectrometer (ICP‐OES). Regression analysis of correlation coefficient (R2) was higher than 0.999 which revealed good linearity. Based on this analysis, the raw vegetables contained 0.20 to 144.98 mg/100 g of sodium, 7.81 to 266.57 mg/100 g of calcium, 230.57 to 812.73 mg/100 g of potassium, 12.16 to 76.28 mg/100 g of magnesium and phosphorus ranged from 35.32 to 123.81 mg/100 g. In addition, the contents of the minerals in the blanched vegetables were 1.40 to 134.75 mg/100 g of sodium, 7.80 to 177.58 mg/100 g of calcium, 150.32 to 651.71 mg/100 g of potassium, 11.17 to 56.63 mg/100 g of magnesium and 36.20 to 136.61 mg/100 g of phosphorus. Hence, it would be expected that the mineral contents could be used to draw up the food nutritional ingredient table.Support or Funding InformationThis work was carried out with the support of “Cooperative Research Program for Agriculture Science &Technology Development (Project No. PJ010846022015)” Rural Development Administration, Republic of Korea.
Immunohistochemical Detection of Autophagy‐Related Proteins in Canine Appendicular Osteosarcoma
Authors: Schott Courtney R. , Wood Geoffrey A. 
Published: November 2023

Dogs diagnosed with appendicular osteosarcoma commonly succumb to metastatic disease despite undergoing the standard of care treatment for curative intent: amputation of the affected limb, followed by adjuvant chemotherapy. Post‐surgical chemotherapy improves one‐ and two‐year survival rates, but prognosis is still poor. In response to adverse environmental conditions normal cells are capable of undergoing autophagy, a survival mechanism involving self‐degradation and recycling of cellular components. Neoplastic cells take advantage of this mechanism to enhance their survival during chemotherapy. Autophagy's role in osteosarcoma has been investigated in humans however similar studies in dogs are rare. Our objective was to examine the expression patterns of a select group of autophagy‐related proteins in canine osteosarcoma amputation samples and to identify potential correlations with survival. Immunohistochemistry for beclin‐1, LC3, phospho‐mTOR, phospho‐AKT1, phospho‐S6 ribosomal protein, and p62 was performed on a tissue microarray containing naïve canine appendicular osteosarcoma cores from dogs who began the standard of care treatment (≥1 dose of chemotherapy). For survival analyses, Kaplan‐Meier survival curves for different expression patterns were compared using the log‐rank test and interactions were considered significant if p < 0.05. The median survival time from the date of diagnosis was 250 days and survival time ranged from 67–897 days (n=20, 95% CI: 122–381). Intense phospho‐S6 ribosomal protein labeling was identified most consistently adjacent to osteoid matrix. Phospho‐mTOR labeling was most evident in the nuclear compartment, however cells undergoing mitosis displayed strong cytoplasmic labeling. Canine osteosarcoma cells exhibited a mixture of diffuse and punctate LC3 cytoplasmic labeling, potentially distinguishing between free cytoplasmic LC3‐I and autophagosome anchored LC3‐II, respectively. Western blot analysis of the beclin‐1 antibody produced a 58 kDa band as predicted. Three distinct intensities of cytoplasmic labeling were observed for beclin‐1 in canine osteosarcoma cells. Strong cytoplasmic beclin‐1 labeling in the majority of neoplastic cells was not observed in any cases with greater than one‐year survival (0/6); this pattern was observed only in cases with less than one‐year survival (5/14). Dogs with tumours having light (n=4), moderate (n=9), and strong (n=5) cytoplasmic labeling had median survival times of 294, 301, and 122 days, respectively. Strong cytoplasmic labeling was a significantly correlated with decreased survival time (Chisq=6.9, 2 df, p < 0.05). This preliminary study provides evidence that canine osteosarcoma cells undergo autophagy in vivo, with a similar LC3 labeling pattern to that described in other tumour types in various species. Additionally, it identifies beclin‐1 as a promising candidate biomarker of chemoresponsiveness in canine appendicular osteosarcoma.Support or Funding InformationFunded by Pet Trust
Ppm1b Negatively Regulates Necroptosis through Dephoshophorylating Rip3
Authors: Jianfeng Wu , wanze Chen , Yangxin Li , Tingting Ai , Jiahuai Han 
Published: November 2023

The auto‐phosphorylation of murine receptor‐interacting protein 3 (Rip3) on Thr‐231 and Ser‐232 in the necrosome is required to trigger necroptosis. We identified protein phosphatase 1B (Ppm1b) as a Rip3 phosphatase and found that Ppm1brestricts necroptosis in two settings: spontaneous necroptosis caused by Rip3auto‐phosphorylation in resting cells, and tumour necrosis factor (TNF)‐α‐induced necroptosis in cultured cells. We revealed that Ppm1b selectively suppresses necroptosis through the dephosphorylation of Rip3, which then prevents the recruitment of mixed lineage kinase domain‐like protein (Mlkl) to the necrosome. We further showed that Ppm1b deficiency (Ppm1b(d/d)) in mice enhanced TNF‐‐α induced death in a Rip3‐dependent manner, and the role of Ppm1bin inhibiting necroptosis was evidenced by elevated Rip3 phosphorylation and tissue damage in the caecum of TNF‐α treated Ppm1b(d/d) mice. We also found epithelial cells in caecum damaged rapidly after TNF‐α treatment. Cecectomy could reverse TNF‐α‐induced death, but not LPS‐induced death in mice. These data indicate that Ppm1b negatively regulates necroptosis through dephosphorylating Rip3 in vitro and in vivo, and epithelial cell necroptosis in caecum may play important roles in several diseases.Support or Funding InformationThis work was supported by the National Basic Research Program of China (973 Program; 2015CB553800), the National Scientific and Technological Major Project (2013ZX10002‐002), the National Natural Science Foundation of China (91429301, 31420103910, 31330047, 91029304, 31221065, and 31090360), the Hi‐Tech Research and Development Program of China (863 program; 2012AA02A201), the 111 Project (B12001), the Science and Technology Foundation of Xiamen (No. 3502Z20130027), the National Science Foundation of China for Fostering Talents in Basic Research (Grant No.J1310027) and the Open Research Fund of State Key Laboratory of Cellular Stress Biology, Xiamen University. This research was also partly supported by grants from MOST (2012CB966600) and NIH (R01GM63773, R01AR053591, R01CA108454).