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#33098750   2020/10/24 To Up

Brachyury engineers cardiac repair competent stem cells.

To optimize the regenerative proficiency of stem cells, a cardiopoietic protein-based cocktail consisting of multiple growth factors has been developed and advanced into clinical trials for treatment of ischemic heart failure. Streamlining the inductors of cardiopoiesis would address the resource intensive nature of the current stem cell enhancement protocol. To this end, the microencapsulated-modified-mRNA (M RNA) technique was here applied to introduce early cardiogenic genes into human adipose-derived mesenchymal stem cells (AMSCs). A single mesodermal transcription factor, Brachyury, was sufficient to trigger high expression of cardiopoietic markers, Nkx2.5 and Mef2c. Engineered cardiopoietic stem cells (eCP) featured a transcriptome profile distinct from pre-engineered AMSCs. In vitro, eCP demonstrated protective antioxidant capacity with enhanced superoxide dismutase expression and activity; a vasculogenic secretome driving angiogenic tube formation; and macrophage polarizing immunomodulatory properties. In vivo, in a murine model of myocardial infarction, intramyocardial delivery of eCP (600 000 cells per heart) improved cardiac performance and protected against decompensated heart failure. Thus, heart repair competent stem cells, armed with antioxidant, vasculogenic, and immunomodulatory traits, are here engineered through a protein-independent single gene manipulation, expanding the available regenerative toolkit.
Mark Li, Satsuki Yamada, Ao Shi, Raman Deep Singh, Tyler J Rolland, Ryounghoon Jeon, Natalia Lopez, Lukas Shelerud, Andre Terzic, Atta Behfar

2575 related Products with: Brachyury engineers cardiac repair competent stem cells.

5 x 10A5 cells/vial10 x 50ul/Unit11 Plate of 96 x 20ul/Unit10 ug1 x 10^6 cells/vial5 x 200ul/Unit100|uI x 10 vials5 x 200ul/Unit100ìl x 10 vials75 x 50ul/Unit10 rxns

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#33098689   2020/10/24 To Up

A mini-Tn5-derived transposon with reportable and selectable markers enables rapid generation and screening of insertional mutants in Gram-negative bacteria.

We re-engineered a classic tool for mutagenesis and gene expression studies in Gram-negative bacteria. Our modified Tn5-based transposon contains multiple features that allow rapid selection for mutants, direct quantification of gene expression, and straightforward cloning of the inactivated gene. The promoter-less gfp-km cassette provides selection and reporter assay depending on the activity of the promoter upstream of the transposon insertion site. The cat gene facilitates positive antibiotic selection for mutants, while the narrow R6Kγ replication origin forces transposition in recipient strains lacking the pir gene and enables cloning the transposon flanked with the disrupted gene from the chromosome. The suicide vector pCKD100, a plasmid that could be delivered into recipient cells through bi-parental mating or electroporation, harbors the modified transposon. We used the transposon to mutagenize Pectobacterium versatile KD100, Pseudumonas coronafaciens PC27R, and Escherichia coli 35150N. The fluorescence intensities of mutants expressing high GFP could be quantified and detected qualitatively. Transformation efficiency from conjugation ranged from 1600 to 1900 CFU ml . We sequenced the upstream flanking regions, identified the putative truncated genes, and demonstrated the restoration of the GFP phenotype through marker exchange. The mini-Tn5 transposon was also utilized to construct mutant library of P. versatile for forward genetic screens.
Eric S Nazareno, Bimala Acharya, C Korsi Dumenyo

1367 related Products with: A mini-Tn5-derived transposon with reportable and selectable markers enables rapid generation and screening of insertional mutants in Gram-negative bacteria.

1 mL400Tests25 mg100ug96T1 ml50 mg100 assays1000 tests

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#33098674   2020/10/24 To Up

The Impact of Vitamin D Status on Cardiometabolic Effects of Fenofibrate in Women with Atherogenic Dyslipidemia.

Vitamin D deficiency is a risk factor for cardiometabolic disease. The aim of this study was to determine the role of vitamin D status in the impact of fenofibrate on plasma levels of cardiometabolic risk factors.The study population (n=61) consisted of threematched groups of women with atherogenic dyslipidemia: vitamin D-naïve women with vitamin D insufficiency (group A), women receiving vitamin D preparations because of vitamin D deficiency (group B), as well as vitamin D-naïve women with normal vitamin D status (group C), who weretreated with micronized fenofibrate (200 mg daily).Glucose homeostasis markers, plasma lipids, as well as plasma levels of 25-hydroxyvitamin D, uric acid, high-sensitivity C-reactive protein (hsCRP), fibrinogen and homocysteine were determined at the beginning of the study and six months later.At entry, group A was characterized by lower levels of 25-hydroxyvitamin D, reduced insulin-sensitivity and higher concentrations of uric acid, hsCRP, fibrinogen and homocysteine. Apart from a weaker effect on HDL-cholesterol and triglycerides in group A, there were no differences between the treatment arms in the effect of fenofibrate on plasma lipids. However, only in groups B and C the drug improved insulin sensitivity and reduced circulating levels of uric acid andhsCRP, as well as increased levels of 25-hydroxyvitamin D and these effects correlated with the degree of improvement in insulin sensitivity. Treatment-induced increase in homocysteine was observed only in group A.The results of the study indicate that cardiometabolic effects of fibrates may depend on the vitamin D status of patients.
Robert Krysiak, Karolina Kowalcze, Bogusław Okopień

2869 related Products with: The Impact of Vitamin D Status on Cardiometabolic Effects of Fenofibrate in Women with Atherogenic Dyslipidemia.

20 100 assays100ug

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#33098662   2020/10/24 To Up

Using RAD-seq to develop sex-linked markers in a haplodiplontic alga.

For many taxa, including isomorphic haplodiplontic macroalgae, determining sex and ploidy is challenging, thereby limiting the scope of some population demographic and genetic studies. Here, we used double digest restriction site-associated DNA sequencing (ddRAD-seq) to identify sex-linked molecular markers in the widespread red alga Agarophyton vermiculophyllum. In the ddRAD-seq library, we included 10 female gametophytes, 10 male gametophytes, and 16 tetrasporophytes from one native and one non-native site (N=40 gametophytes and N=32 tetrasporophytes total). We identified seven putatively female-linked and 19 putatively male-linked sequences. Four female- and eight male-linked markers amplified in all three life cycle stages. Using one female- and one male-linked marker that were sex-specific, we developed a duplex PCR and tested the efficacy of this assay on a subset of thalli sampled at two sites in the non-native range. We confirmed ploidy based on the visual observation of reproductive structures and previous microsatellite genotyping at 10 polymorphic loci. For 32 vegetative thalli, we were able to assign sex and confirm ploidy in these previously genotyped thalli. These markers will be integral to on-going studies of A. vermiculophyllum invasion. We discuss the utility of RAD-seq over other approaches previously used, such as RAPDs (random amplified polymorphic DNA), for future work designing sex-linked markers in other haplodiplontic macroalgae for which genomes are lacking.
Stacy A Krueger-Hadfield, Ben A Flanagan, Olivier Godfroy, Kristina M Hill-Spanik, Chris C Nice, Courtney J Murren, Allan E Strand, Erik E Sotka

2178 related Products with: Using RAD-seq to develop sex-linked markers in a haplodiplontic alga.

1 kit100 ug1 kit300 units0.1ml (1mg/ml)

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#33098644   2020/10/24 To Up

11βHSD1 inhibition with AZD4017 improves lipid profiles and lean muscle mass in Idiopathic intracranial hypertension.

The enzyme 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) determines pre-receptor metabolism and activation of glucocorticoids within peripheral tissues. Its dysregulation has been implicated in a wide array of metabolic diseases, leading to the development of selective 11β-HSD1 inhibitors. We examined the impact of the reversible competitive 11β-HSD1 inhibitor, AZD4017, on the metabolic profile in an overweight female cohort with idiopathic intracranial hypertension.
Rowan S Hardy, Hannah Botfield, Keira Markey, James L Mitchell, Zerin Alimajstorovic, Connar S J Westgate, Michael Sagmeister, Rebecca J Fairclough, Ryan S Ottridge, Andreas Yiangou, Karl-Heinz H Storbeck, Angela E Taylor, Lorna C Gilligan, Wiebke Arlt, Paul M Stewart, Jeremy W Tomlinson, Susan P Mollan, Gareth G Lavery, Alexandra J Sinclair

2771 related Products with: 11βHSD1 inhibition with AZD4017 improves lipid profiles and lean muscle mass in Idiopathic intracranial hypertension.

0.1ml (1mg/ml)96 assays 48 assays 96 assays 96 wells48 assays48 assays 96 wells

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#33098601   2020/10/24 To Up

Comprehensive phenotyping of peripheral blood T lymphocytes in healthy mice.

T lymphocytes play a central role in antigen-specific immune responses. They modulate the function of different immune cells both through a direct contact (receptor binding) and through the secretion of cytokines. At the same time, they are deeply involved in the direct killing of aberrant target cells. T lymphocytes derive from a bone marrow precursor that migrates in the thymus where the main differentiation steps take place. Mature CD4 and CD8 single-positive cells, then, leave the thymus to reach the secondary lymphoid organs. T cell subsets and their maturation steps can be identified mainly based on the expression of extracellular markers, intracellular transcription factors and cytokine production profiles. In this review, we report, from a cytometric point of view, an overview of the most important T cell subpopulations and their differentiation state.
Genny Del Zotto, Elisa Principi, Francesca Antonini, Serena Baratto, Chiara Panicucci, Claudio Bruno, Lizzia Raffaghello

1696 related Products with: Comprehensive phenotyping of peripheral blood T lymphocytes in healthy mice.

100 extractions96 tests100 μg1 kit251mg1 Set

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#33098599   2020/10/24 To Up

Tempol improves redox status in mdx dystrophic diaphragm muscle.

Oxidative stress is a critical element in relationship to the pathophysiology of Duchenne muscular dystrophy (DMD). In the mice the diaphragm (DIA) is most resembles the dystrophic human pathology. In this study we have evaluated the consequences of a synthetic antioxidant (tempol) on oxidative stress parameters in the DIA muscle of mdx mice. The mdx mice were separated into two groups: mdx, the control group receiving intraperitoneal (i.p.) injections of saline solution (100 µL), and mdxT, the treated group receiving i.p. injections of tempol (100 mg/kg). The tempol-treated group showed reduced oxidative stress markers, decreasing the dihydroethidium reaction (DHE) area; autofluorescent lipofuscin granules; and 4-hydroxynonenal (4-HNE)-protein adduct levels. DIA muscle of mdx mice. At the same time, the manganese-superoxide dismutase 2 (SOD2) levels were increased in the tempol-treated group. In addition, the tempol-treated group showed reduced levels of glutathione-disulphide reductase (GSR), glutathione peroxidase 1 (GPx1) and catalase (CAT) in immunoblots. The tempol-treated group has also shown lower relative gene expression of SOD1, CAT and GPx than the non-treated group. Our data demonstrated that tempol treatment reduced oxidant parameters and increased anti-oxidant SOD2 levels in the DIA muscle of mdx mice, which may contribute to the normalization of the redox homeostasis of dystrophic muscles.
Túlio de Almeida Hermes, Daniela Sayuri Mizobuti, Guilherme Luiz da Rocha, Heloina Nathalliê Mariano da Silva, Caroline Covatti, Elaine Cristina Leite Pereira, Renato Ferretti, Elaine Minatel

2224 related Products with: Tempol improves redox status in mdx dystrophic diaphragm muscle.

100 ml.25 ml.96 wells96 wells1 set (5 x 1 ml)100 μg100 μg1 mg

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