Tag: M.W=300-350

Jiang, Lin published the artcileCRISPR activation of endogenous genes reprograms fibroblasts into cardiovascular progenitor cells for myocardial infarction therapy, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the publication is Molecular Therapy (2022), 30(1), 54-74, database is CAplus and MEDLINE.

Fibroblasts can be reprogrammed into cardiovascular progenitor cells (CPCs) using transgenic approaches, although the underlying mechanism remains unclear. We determined whether activation of endogenous genes such as Gata4, Nkx2.5, and Tbx5 can rapidly establish autoregulatory loops and initiate CPC generation in adult extracardiac fibroblasts using a CRISPR activation system. The induced fibroblasts (>80%) showed phenotypic changes as indicated by an Nkx2.5 cardiac enhancer reporter. The progenitor characteristics were confirmed by colony formation and expression of cardiovascular genes. Cardiac sphere induction segregated the early and late reprogrammed cells that can generate functional cardiomyocytes and vascular cells in vitro. Therefore, they were termed CRISPR-induced CPCs (ciCPCs). Transcriptomic anal. showed that cell cycle and heart development pathways were important to accelerate CPC formation during the early reprogramming stage. The CRISPR system opened the silenced chromatin locus, thereby allowing transcriptional factors to access their own promoters and eventually forming a pos. feedback loop. The regenerative potential of ciCPCs was assessed after implantation in mouse myocardial infarction models. The engrafted ciCPCs differentiated into cardiovascular cells in vivo but also significantly improved contractile function and scar formation. In conclusion, multiplex gene activation was sufficient to drive CPC reprogramming, providing a new cell source for regenerative therapeutics.

Molecular Therapy published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Li, Yakun published the artcileSuper-structural 2D ultrathin carbon nitride/acrylate boron silane polymer with multi-function for enhancing antifouling performance, Recommanded Product: Triphenyl(pyridin-1-ium-1-yl)borate, the publication is Journal of Coatings Technology and Research (2021), 18(4), 1051-1064, database is CAplus.

Haunted by marine biofouling and the ecol. crisis caused by toxic antifouling paints, the demand for environmental coatings has become more and more pressing. In this work, a series of super-structural 2D ultrathin carbon nitride/acrylate boron silane polymers (CNPs) was prepared by incorporating C₃N₄ into a self-polishing acrylate boron silane polymer (ABSP). The antifouling, environmental performances were evaluated, and the antifouling mechanism was investigated. The results showed that when the content of C₃N₄ was 3-7 wt%, the coatings showed the best resistance to diatoms, Staphylococcus aureus and Escherichia coli in visible light. It was noted that the coatings showed weak antibacterial properties in the dark. In addition, the CNPs and ABSP were shown to expel mussels by photocatalytic active species, self-renewal and amphiphilic surfaces. The COD (COD) values showed that the addition of C₃N₄ made the CNPs become environmental coatings.

Journal of Coatings Technology and Research published new progress about 971-66-4. 971-66-4 belongs to pyridine-derivatives, auxiliary class Pyridine,Benzene, name is Triphenyl(pyridin-1-ium-1-yl)borate, and the molecular formula is C23H20BN, Recommanded Product: Triphenyl(pyridin-1-ium-1-yl)borate.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Tung, Ying-Chang published the artcileComparative effectiveness of generic nifedipine versus Adalat long-acting nifedipine for hypertension treatment: A multi-institutional cohort study, Product Details of C17H18N2O6, the publication is Journal of Clinical Hypertension (Hoboken, NJ, United States) (2022), 24(5), 621-629, database is CAplus and MEDLINE.

This retrospective multi-institutional database anal. aimed to evaluate the blood-pressure-lowering efficacy and clin. outcomes of a generic vs. brand-name nifedipine for hypertension management. A total of 12 693 patients who were prescribed a generic or brand-name nifedipine between Jan. 1, 2011, and Dec. 31, 2018, were identified from the Chang Gung Research Database of Chang Gung Memorial Hospitals, Taiwan. Among them, 2112 (21.4%) were prescribed generic nifedipine. After propensity score matching, both the generic and brand-name groups consisted of 2102 patients. At a mean follow-up of 3 years, the changes in office systolic (p for interaction = .791) and diastolic blood pressure (p for interaction = .689) did not differ significantly between the patients who received the generic and the brand-name nifedipine. There was no significant difference between the two study groups regarding the composite of all-cause mortality, acute myocardial infarction, stroke, coronary revascularization, or hospitalization for heart failure (hazard ratio 0.98, 95% confidence interval 0.85-1.13; p = .774). In conclusion, the generic nifedipine was comparable to its brand-name counterpart regarding office blood pressure reduction and the composite cardiovascular outcome for the treatment of patients with hypertension.

Journal of Clinical Hypertension (Hoboken, NJ, United States) published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C6H6BClO3, Product Details of C17H18N2O6.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Wolf, William J. published the artcileExamining the Effects of Monomer and Catalyst Structure on the Mechanism of Ruthenium-Catalyzed Ring-Opening Metathesis Polymerization, Product Details of C23H20BN, the publication is Journal of the American Chemical Society (2019), 141(44), 17796-17808, database is CAplus and MEDLINE.

The mechanism of Ru-catalyzed ring-opening metathesis polymerization (ROMP) is studied in detail using a pair of third generation ruthenium catalysts with varying sterics of the N-heterocyclic carbene (NHC) ligand. Exptl. evidence for polymer chelation to the Ru center is presented in support of a monomer-dependent mechanism for polymerization of norbornene monomers using these fast-initiating catalysts. A series of kinetic experiments, including rate measurements for ROMP, rate measurements for initiation, monomer-dependent kinetic isotope effects, and activation parameters were useful for distinguishing chelating and nonchelating monomers and determining the effect of chelation on the polymerization mechanism. The formation of a chelated metallacycle is enforced by both the steric bulk of the NHC and by the geometry of the monomer, leading to a ground-state stabilization that slows the rate of polymerization and also alters the reactivity of the propagating Ru center toward different monomers in copolymerizations The results presented here add to the body of mechanistic work for olefin metathesis and may inform the continued design of catalysts for ROMP to access new polymer architectures and materials.

Journal of the American Chemical Society published new progress about 971-66-4. 971-66-4 belongs to pyridine-derivatives, auxiliary class Pyridine,Benzene, name is Triphenyl(pyridin-1-ium-1-yl)borate, and the molecular formula is C9H10O4, Product Details of C23H20BN.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Beraki, Simret published the artcileA pharmacological screening approach for discovery of neuroprotective compounds in ischemic stroke, Category: pyridine-derivatives, the publication is PLoS One (2013), 8(7), e69233, database is CAplus and MEDLINE.

With the availability and ease of small mol. production and design continuing to improve, robust, high-throughput methods for screening are increasingly necessary to find pharmacol. relevant compounds amongst the masses of potential candidates. Here, we demonstrate that a primary oxygen glucose deprivation assay in primary cortical neurons followed by secondary assays (i.e. post-treatment protocol in organotypic hippocampal slice cultures and cortical neurons) can be used as a robust screen to identify neuroprotective compounds with potential therapeutic efficacy. In our screen about 50% of the compounds in a library of pharmacol. active compounds displayed some degree of neuroprotective activity if tested in a pre-treatment toxicity assay but just a few of these compounds, including Carbenoxolone, remained active when tested in a post-treatment protocol. When further examined, Carbenoxolone also led to a significant reduction in infarction size and neuronal damage in the ischemic penumbra when administered six hours post middle cerebral artery occlusion in rats. Pharmacol. testing of Carbenoxolone-related compounds, acting by inhibition of 11-β-hydroxysteroid dehydrogenase-1 (11β-HSD1), gave rise to similarly potent in vivo neuroprotection. This indicates that the increase of intracellular glucocorticoid levels mediated by 11β-HSD1 may be involved in the mechanism that exacerbates ischemic neuronal cell death and inhibiting this enzyme could have potential therapeutic value for neuroprotective therapies in ischemic stroke and other neurodegenerative disorders associated with neuronal injury.

PLoS One published new progress about 54856-23-4. 54856-23-4 belongs to pyridine-derivatives, auxiliary class Pyridine,Salt,Amine,Inhibitor,Inhibitor, name is N-Methyl-2-(pyridin-2-yl)ethan-1-amine dimethanesulfonate, and the molecular formula is C10H20N2O6S2, Category: pyridine-derivatives.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Bertagna, Federico published the artcileThapsigargin blocks electromagnetic field-elicited intracellular Ca²⁺ increase in HEK 293 cells, Computed Properties of 21829-25-4, the publication is Physiological Reports (2022), 10(9), e15189, database is CAplus and MEDLINE.

Biol. effects of electromagnetic fields (EMFs) have previously been identified for cellular proliferation and changes in expression and conduction of diverse types of ion channels. The major effect elicited by EMFs seems to be directed toward Ca2+ homeostasis. This is particularly remarkable since Ca2+ acts as a central modulator in various signaling pathways, including, but not limited to, cell differentiation and survival. Despite this, the mechanisms underlying this modulation have yet to be unraveled. Here, we assessed the effect of EMFs on intracellular [Ca2+], by exposing HEK 293 cells to both radio-frequency electromagnetic fields (RF-EMFs) and static magnetic fields (SMFs). We detected a constant and significant increase in [Ca2+] subsequent to exposure to both types of fields. Strikingly, the increase was nulled by administration of 10 μM Thapsigargin, a blocker of sarco/endoplasmic reticulum Ca2+-ATPases (SERCAs), indicating the involvement of the endoplasmic reticulum (ER) in EMF-related modulation of Ca2+ homeostasis.

Physiological Reports published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Computed Properties of 21829-25-4.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Zhang, Zixu published the artcilePhotocatalytic antifouling coating based on carbon nitride with dynamic acrylate boron fluorinated polymers, Product Details of C23H20BN, the publication is New Journal of Chemistry (2021), 45(2), 780-787, database is CAplus.

Based on the situation of marine biofouling and the ecol. crisis caused by toxic antifouling paints, a series of environmental carbon nitride (C₃N₄) nanocomposite films (CNPs) were prepared by incorporating C₃N₄ into a self-polishing acrylate boron fluorinated polymer (ABFP). The antifouling performance was evaluated by the diatom anti-attachment test, photocatalytic antibacterial measurements and a mussel settlement assay. The results showed that the optimal content of C₃N₄ to inhibit the adhesion of diatoms was 3-7 wt%, the antibacterial rate of Staphylococcus aureus (S. aureus) and Escherichia coli (E. coli) reached 98.10% and 96.94% in the presence of 7 wt% C₃N₄ under irradiation with visible light for 90 min. In addition, the CNPs and ABFP showed an ability to expel mussels. As a synergistic effect, the self-renewable polymer surfaces could also strip the attached fouling organisms without light. The undifferentiated growth rates between the CNPs and blank proved the environmental properties of the prepared films. The COD values showed that the addition of C₃N₄ contributed to the eco-friendly properties of the CNPs.

New Journal of Chemistry published new progress about 971-66-4. 971-66-4 belongs to pyridine-derivatives, auxiliary class Pyridine,Benzene, name is Triphenyl(pyridin-1-ium-1-yl)borate, and the molecular formula is C7H11N, Product Details of C23H20BN.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Li, Shikai published the artcileInhibition of Sympathetic Activation by Delivering Calcium Channel Blockers from a 3D Printed Scaffold to Promote Bone Defect Repair, Related Products of pyridine-derivatives, the publication is Advanced Healthcare Materials (2022), 11(16), 2200785, database is CAplus and MEDLINE.

Enhancing osteogenesis by promoting neural network reconstruction and neuropeptide release is considered to be an attractive strategy for repairing of critical size bone defects. However, traumatic bone defects often activate the damaged sympathetic nervous system (SNS) in the defect area and release excessive catecholamine to hinder bone defect repair. Herein, a 3D printed scaffold loaded with the calcium channel blocker-nifedipine is proposed to reduce the concentration of catecholamine present in the bone defect region and to accelerate bone healing. To this end, nifedipine-loaded ethosome and laponite are added into a mixed solution containing sodium alginate, methacrylated gelatin, and bone mesenchymal stem cells (BMSCs) to prepare a cell-laden scaffold using 3D bioprinting. The released nifedipine is able to close the calcium channels of nerve cells, thereby blocking sympathetic activation and ultimately inhibiting the release of catecholamine by sympathetic nerve cells, which further promotes the osteogenic differentiation and migration of BMSCs, inhibits osteoclastogenesis in vitro, and effectively improves bone regeneration in a rat critical-size calvarial defect model. Therefore, the results suggest that sustained release of nifedipine from the scaffold can effectively block SNS activation, providing promising strategies for future treatment of bone defects.

Advanced Healthcare Materials published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Related Products of pyridine-derivatives.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Yang, Biao published the artcileA conductive supramolecular hydrogel creates ideal endogenous niches to promote spinal cord injury repair, Product Details of C17H18N2O6, the publication is Bioactive Materials (2022), 103-119, database is CAplus and MEDLINE.

The current effective method for treatment of spinal cord injury (SCI) is to reconstruct the biol. microenvironment by filling the injured cavity area and increasing neuronal differentiation of neural stem cells (NSCs) to repair SCI. However, the method is characterized by several challenges including irregular wounds, and mech. and elec. mismatch of the material-tissue interface. In the current study, a unique and facile agarose/gelatin/polypyrrole (Aga/Gel/PPy, AGP3) hydrogel with similar conductivity and modulus as the spinal cord was developed by altering the concentration of Aga and PPy. The gelation occurred through non-covalent interactions, and the phys. crosslinked features made the AGP3 hydrogels injectable. In vitro cultures showed that AGP3 hydrogel exhibited excellent biocompatibility, and promoted differentiation of NSCs toward neurons whereas it inhibited over-proliferation of astrocytes. The in vivo implanted AGP3 hydrogel completely covered the tissue defects and reduced injured cavity areas. In vivo studies further showed that the AGP3 hydrogel provided a biocompatible microenvironment for promoting endogenous neurogenesis rather than glial fibrosis formation, resulting in significant functional recovery. RNA sequencing anal. further indicated that AGP3 hydrogel significantly modulated expression of neurogenesis-related genes through intracellular Ca2+ signaling cascades. Overall, this supramol. strategy produces AGP3 hydrogel that can be used as favorable biomaterials for SCI repair by filling the cavity and imitating the physiol. properties of the spinal cord.

Bioactive Materials published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C9H11BO4, Product Details of C17H18N2O6.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem

Ulivieri, Alessandra published the artcileThyroid hormones regulate cardiac repolarization and QT-interval related gene expression in hiPSC cardiomyocytes, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the publication is Scientific Reports (2022), 12(1), 568, database is CAplus and MEDLINE.

Prolongation of cardiac repolarization (QT interval) represents a dangerous and potentially life-threatening elec. event affecting the heart. Thyroid hormones (THs) are critical for cardiac development and heart function. However, little is known about THs influence on ventricular repolarization and controversial effects on QT prolongation are reported. Human iPSC-derived cardiomyocytes (hiPSC-CMs) and multielectrode array (MEA) systems were used to investigate the influence of 3,3′,5-triiodo-L-Thyronine (T3) and 3,3′,5,5′-tetraiodo-L-Thyronine (T4) on corrected Field Potential Duration (FPDc), the in vitro analog of QT interval, and on local extracellular Action Potential Duration (APD). Treatment with high THs doses induces a significant prolongation of both FPDc and APD, with the strongest increase reached after 24 h exposure. Preincubation with reverse T3 (rT3), a specific antagonist for nuclear TH receptor binding, significantly reduces T3 effects on FPDc, suggesting a TRs-mediated transcriptional mechanism. RNA-seq anal. showed significant deregulation in genes involved in cardiac repolarization pathways, including several QT-interval related genes. In conclusion, long-time administration of high THs doses induces FPDc prolongation in hiPSC-CMs probably through the modulation of genes linked to QT-interval regulation. These results open the way to investigate new potential diagnostic biomarkers and specific targeted therapies for cardiac repolarization dysfunctions.

Scientific Reports published new progress about 21829-25-4. 21829-25-4 belongs to pyridine-derivatives, auxiliary class Membrane Transporter/Ion Channel,Calcium Channel, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C9H5Cl2F3, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
https://en.wikipedia.org/wiki/Pyridine,
Pyridine | C5H5N – PubChem