Day: December 21, 2022

Liu, Xiaoxi published the artcileRegulating Molecular Recognition with C-Shaped Strips Attained by Chirality-Assisted Synthesis, Safety of 1,1-Di-n-octyl-4,4-bipyridinium Dibromide, the main research area is chirality assisted synthesis mol recognition mol shape strip; chirality-assisted synthesis; cooperative effects; host-guest interactions; shape control; supramolecular chemistry.

Chirality-assisted synthesis (CAS) is a general approach to control the shapes of large mol. strips. CAS is based on enantiomerically pure building blocks that are designed to strictly couple in a single geometric orientation. Fully shape-persistent structures can thus be created, even in the form of linear chains. With CAS, selective recognition between large host and guest mols. can reliably be designed de novo. To demonstrate this concept, three C-shaped strips that can embrace a pillar[5]arene macrocycle were synthesized. The pillar[5]arene bound to the strips was a better host for electron-deficient guests than the free macrocycle. Exptl. and computational evidence is provided for these unique cooperative interactions to illustrate how CAS could open the door towards the precise positioning of functional groups for regulated supramol. recognition and catalysis.

Angewandte Chemie, International Edition published new progress about Chirality. 36437-30-6 belongs to class pyridine-derivatives, name is 1,1-Di-n-octyl-4,4-bipyridinium Dibromide, and the molecular formula is C26H42Br2N2, Safety of 1,1-Di-n-octyl-4,4-bipyridinium Dibromide.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Croitoru, M. D. published the artcileDirect HPLC-UV determination of cyclemate, saccharine and aspartame from soft drinks, Recommanded Product: Ethyl 4-hydroxy-6-oxo-6,7-dihydrothieno[2,3-b]pyridine-5-carboxylate, the main research area is cyclamate saccharine aspartame soft drink HPLC UV detection.

Artificial sweeteners were introduced in therapy as sugar substitutes for diabetic patients. Nowadays these substances are widely used for sugar substitution in low calorie drinks and sweets. Most commonly used products to date are saccharine, cyclamate, aspartame, and acesulfam; maximum accepted daily intakes are stated for each one. A simple reverse phase (RP18) HPLC-UV method with direct detection (196 nm) was developed by us in order to measure the concentrations of the three sweeteners. No sample preparation is required, other than dilution Limits of detection are 12 mg l-1, 0.5 mg l-1 and lower than 0.25 mg l-1 for cyclamate, aspartame and saccharine, resp. Concentrations ranged between 113.14-280.07 mg l-1 in the case of cyclamate, 17.96-50.94 mg l-1 for saccharine, and 9.94-296.82 mg l-1 for aspartame.

Acta Alimentaria published new progress about Beverages. 99429-68-2 belongs to class pyridine-derivatives, name is Ethyl 4-hydroxy-6-oxo-6,7-dihydrothieno[2,3-b]pyridine-5-carboxylate, and the molecular formula is C10H9NO4S, Recommanded Product: Ethyl 4-hydroxy-6-oxo-6,7-dihydrothieno[2,3-b]pyridine-5-carboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Kim, Seul Gi published the artcileNifedipine-induced AMPK activation alleviates senescence by increasing autophagy and suppressing of Ca2+ levels in vascular smooth muscle cells, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is vascular smooth muscle cell senescence autophagy calcium AMPK nifedipine; AMPK; Autophagy; Ca(2+); Nifedipine; Senescence; Vascular smooth muscle cell.

Calcium (Ca2+) homeostasis is disrupted during aging in several cell types and this disruption leads to autophagy impairment. The mechanisms regarding Ca2+, senescence, and autophagy need to be elucidated. Therefore, we hypothesized that cellular senescence can be improved by regulating Ca2+ level and autophagy activity. We identified that hydrogen peroxide (H2O2)-induced senescence was accompanied by Ca2+ elevation, impairment of autophagic flux and increase of mammalian target of rapamycin (mTOR) phosphorylation in VSMCs. The treatment of nifedipine dose-dependently suppressed H2O2-induced senescence by reducing Ca2+ entry, autophagy impairment and mTOR signaling, and this suppression was found to be related to senescence-associated β-galactosidase (SA-β-gal) activity and the expressions of senescence marker protein 30 (SMP30), p53, and p21. Furthermore, H2O2-induced autophagy impairment also accelerated senescence and accumulations of ubiquitinated proteins. AMPK inhibition or transfection with AMPK siRNA showed that the anti-senescence effect of nifedipine involved AMPK activation. These results suggest nifedipine-inducted AMPK activation suppresses VSMC senescence by regulating autophagic flux and Ca2+ levels.

Mechanisms of Ageing and Development published new progress about Autophagy. 21829-25-4 belongs to class pyridine-derivatives, 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:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Laryushkin, Denis P. published the artcileRole of L-Type Voltage-Gated Calcium Channels in Epileptiform Activity of Neurons, Related Products of pyridine-derivatives, the main research area is voltage gated calcium channel neuron epileptiform activity; diltiazem; epileptiform activity; isradipine; neurons; nifedipine; paroxysmal depolarization shift; verapamil; voltage-gated calcium channels.

Epileptic discharges manifest in individual neurons as abnormal membrane potential fluctuations called paroxysmal depolarization shift (PDS). PDSs can combine into clusters that are accompanied by synchronous oscillations of the intracellular Ca2+ concentration ([Ca2+]i) in neurons. Here, we investigate the contribution of L-type voltage-gated calcium channels (VGCC) to epileptiform activity induced in cultured hippocampal neurons by GABA(A)R antagonist, bicuculline. Using KCl-induced depolarization, we determined the optimal EDs of the blockers. Dihydropyridines (nifedipine and isradipine) at concentrations â‰?10μM demonstrate greater selectivity than the blockers from other groups (phenylalkylamines and benzothiazepines). However, high doses of dihydropyridines evoke an irreversible increase in [Ca2+]i in neurons and astrocytes. In turn, verapamil and diltiazem selectively block L-type VGCC in the range of 1-10μM, whereas high doses of these drugs block other types of VGCC. We show that L-type VGCC blockade decreases the half-width and amplitude of bicuculline-induced [Ca2+]i oscillations. We also observe a decrease in the number of PDSs in a cluster and cluster duration. However, the pattern of individual PDSs and the frequency of the cluster occurrence change insignificantly. Thus, our results demonstrate that L-type VGCC contributes to maintaining the required [Ca2+]i level during oscillations, which appears to determine the number of PDSs in the cluster.

International Journal of Molecular Sciences published new progress about Astrocyte. 21829-25-4 belongs to class pyridine-derivatives, 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:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Lu, Yao published the artcileDevelopment of a two-layer transwell co-culture model for the in vitro investigation of pyrrolizidine alkaloid-induced hepatic sinusoidal damage, SDS of cas: 21829-25-4, the main research area is pyrrolizidine alkaloid hepatic sinusoidal damage transwell culture; HepaRG hepatocytes; Hepatic sinusoidal damage; In vitro cell model; Pyrrolizidine alkaloid; Transwell co-culture model.

Pyrrolizidine alkaloids (PAs) are hepatotoxic and specifically damage hepatic sinusoidal endothelial cells (HSECs) via cytochrome P 450 enzymes (CYPs)-mediated metabolic activation. Due to the lack of CYPs in HSECs, currently there is no suitable cell model for investigating PA-induced HSEC injury. This study aimed to establish a two-layer transwell co-culture model that mimics hepatic environment by including HepaRG hepatocytes and HSECs to evaluate cytotoxicity of PAs on their major target HSECs. In this model, PAs were metabolically activated by CYPs in HepaRG hepatocytes to generate reactive pyrrolic metabolites, which react with co-cultured HSECs leading to HSEC damage. Three representative PAs, namely retrorsine, monocrotaline, and clivorine, induced significant concentration-dependent cytotoxicity in HSECs in the co-culture model, but did no cause obvious cytotoxicity directly in HSECs. Using the developed co-cultured model, further mechanism studies of retrorsine-induced HSEC damage demonstrated that the reactive pyrrolic metabolite generated by CYP-mediated bioactivation in HepaRG hepatocytes caused formation of pyrrole-protein adducts, reduction of GSH content, and generation of reactive oxygen species in HSECs, leading to cell apoptosis. The established co-culture model is reliable and applicable for cytotoxic assessment of PA-induced HSEC damage and offers a novel platform for screening toxicity of different PAs on their target cells.

Food and Chemical Toxicology published new progress about Apoptosis. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, SDS of cas: 21829-25-4.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Bayer, Robin published the artcileMechano-pharmacological testing of L-type Ca2+ channel modulators via human vascular celldrum model, Application In Synthesis of 21829-25-4, the main research area is verapamil antioxidant calcium channel agonist smooth muscle cell stress; Celldrum; Biomechanics; Mechanobiology; Human arterial smooth muscle cells (haSMC); Vasoconstriction; Vasopressors; Vasoactive agents.

This study aimed to establish a precise and well-defined working model, assessing pharmaceutical effects on vascular smooth muscle cell monolayer in-vitro. This study focuses on the dilative and contractive effects of L-type Ca2+ channel agonists and antagonists, resp. We analyzed the effects of Bay K8644, nifedipine and verapamil. Three different measurement modes were developed and applied to determine the most appropriate anal. technique for the study purpose. These three operation modes are called, particular time mode, long term mode and real-time mode. It was possible to quantify the biomech. response of haSMCs to the addition of vasoactive agents using CellDrum technol. Due to the supplementation of 100nM Bay K8644, the tension increased approx. 10.6% from initial tension maximum, whereas, the treatment with nifedipine and verapamil caused a significant decrease in cellular tension: 10nM nifedipine decreased the biomech. stress around 6,5% and 50nM verapamil by 2,8%, compared to the initial tension maximum Addnl., all tested measurement modes provide similar results while focusing on different anal. parameters. Conclusion: The CellDrum technol. allows highly sensitive biomech. stress measurements of cultured haSMC monolayers. The mech. stress responses evoked by the application of vasoactive calcium channel modulators were quantified functionally (N/m2). All tested operation modes resulted in equal findings, whereas each mode features operation-related data anal.

Cellular Physiology & Biochemistry published new progress about Apoptosis. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Application In Synthesis of 21829-25-4.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Santos, S. published the artcileBryophyllum pinnatum enhances the inhibitory effect of atosiban and nifedipine on human myometrial contractility: an in vitro study, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is Bryophyllum atosiban nifedipine human myometrial contractility; Atosiban; Bryophyllum pinnatum; Contractility; Myometrium; Nifedipine; Preterm.

The herbal medicine Bryophyllum pinnatum has been used as a tocolytic agent in anthroposophic medicine and, recently, in conventional settings alone or as an add-on medication with tocolytic agents such as atosiban or nifedipine. We wanted to compare the inhibitory effect of atosiban and nifedipine on human myometrial contractility in vitro in the absence and in the presence of B. pinnatum press juice (BPJ). Myometrium biopsies were collected during elective Caesarean sections. Myometrial strips were placed under tension into an organ bath and allowed to contract spontaneously. Test substances alone and at concentrations known to moderately affect contractility in this setup, or in combination, were added to the organ bath, and contractility was recorded throughout the experiments Changes in the strength (measured as area under the curve (AUC) and amplitude) and frequency of contractions after the addition of all test substances were determined Cell viability assays were performed with the human myometrium hTERT-C3 and PHM1-41 cell lines. BPJ (2.5μg/mL), atosiban (0.27μg/mL), and nifedipine (3 ng/mL), moderately reduced the strength of spontaneous myometrium contractions. When BPJ was added together with atosiban or nifedipine, inhibition of contraction strength was significantly higher than with the tocolytics alone (p = 0.03 and p < 0.001, resp.). In the case of AUC, BPJ plus atosiban promoted a decrease to 48.8 ± 6.3% of initial, whereas BPJ and atosiban alone lowered it to 70.9 ± 4.7% and to 80.9 ± 4.1% of initial, resp. Also in the case of AUC, BPJ plus nifedipine promoted a decrease to 39.9 ± 4.6% of initial, at the same time that BPJ and nifedipine alone lowered it to 78.9 ± 3.8% and 71.0 ± 3.4% of initial. Amplitude data supported those AUC data. The inhibitory effects of BPJ plus atosiban and of BPJ plus nifedipine on contractions strength were concentration-dependent. None of the test substances, alone or in combination, decreased myometrial cell viability. BPJ enhances the inhibitory effect of atosiban and nifedipine on the strength of myometrial contractions, without affecting myometrium tissue or cell viability. The combination treatment of BPJ with atosiban or nifedipine has therapeutic potential. BMC Complementary and Alternative Medicine published new progress about Apoptosis. 21829-25-4 belongs to class pyridine-derivatives, 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:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Chovancova, Barbora published the artcileCalcium signaling affects migration and proliferation differently in individual cancer cells due to nifedipine treatment, Computed Properties of 21829-25-4, the main research area is calcium signaling cancer migration proliferation nifedipine; Apoptosis; Breast cancer; Inositol 1,4,5-trisphosphate receptor; Migration; Sodium calcium exchanger 1.

Several papers have reported that calcium channel blocking drugs were associated with increased breast cancer risk and worsened prognosis. One of the most common signs of breast tumors is the presence of small deposits of calcium, known as microcalcifications. Therefore, we studied the effect of dihydropyridine nifedipine on selected calcium transport systems in MDA-MB-231 cells, originating from triple neg. breast tumor and JIMT1 cells that represent a model of HER2-pos. breast cancer, which possesses amplification of HER2 receptor, but cells do not response to HER2 inhibition treatment with trastuzumab. Also, we compared the effect of nifedipine on colorectal DLD1 and ovarian A2780 cancer cells. Both, inositol 1,4,5-trisphosphate receptor type 1 (IP3R1) and type 1 sodium calcium exchanger (NCX1) were upregulated due to nifedipine in DLD1 and A2780 cells, but not in breast cancer MDA-MB-231 and JIMT1 cells. On contrary to MDA-MB-231 and JIMT1 cells, in DLD1 and A2780 cells nifedipine induced apoptosis in a concentration-dependent manner. After NCX1 silencing and subsequent treatment with nifedipine, proliferation was decreased in MDA-MB-231, increased in DLD1 cells, and not changed in JIMT1 cells. Silencing of IP3R1 revealed increase in proliferation in DLD1 and JIMT1 cells, but caused decrease in proliferation in MDA-MB-231 cell line after nifedipine treatment. Interestingly, after nifedipine treatment migration was not significantly affected in any of tested cell lines after NCX1 silencing. Due to IP3R1 silencing, significant decrease in migration occurred in MDA-MB-231 cells after nifedipine treatment, but not in other tested cells. These results support different function of the NCX1 and IP3R1 in the invasiveness of various cancer cells due to nifedipine treatment.

Biochemical Pharmacology (Amsterdam, Netherlands) published new progress about Apoptosis. 21829-25-4 belongs to class pyridine-derivatives, 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:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Segura-Chama, Pedro published the artcileModulation of intracellular calcium concentration by D2-like DA receptor agonists in non-peptidergic DRG neurons is mediated mainly by D4 receptor activation, Quality Control of 21829-25-4, the main research area is calcium DA receptor DRG neuron D4receptor; Ca(2+) microfluorometry; Ca(V)2.2 Ca(2+) channels; D2-like receptors; D4 receptor; Depolarization-elicited [Ca(2+)](i) increase; Small non-peptidergic DRG neurons.

Nociceptive stimuli attributes are codified in the periphery; at this level, D2-like dopamine (DA) receptor activation decreases the high voltage-gated Ca2+ current predominantly in mechanonociceptive neurons, which explains the presynaptic action mechanism of the antinociception produced by quinpirole when it is intrathecally administered in rats. However, the identity of D2-like DA receptor subtype that mediates this effect remains unknown. To answer this question, we used Fluo-4-based Ca2+ microfluorometry to study the depolarization-elicited [Ca2+]i increase in small non-peptidergic DRG neurons (identified by its binding to the Isolectin B4), and to test the effect of D2-like DA receptor activation by quinpirole in presence of selective antagonists for D2, D3, and D4 DA receptors. The results showed a significantly greater contribution of the D4 DA receptor in the down-modulation of depolarization-elicited [Ca2+]i increase in small non-peptidergic DRG neurons compared to the other receptors. Although the D2 and D3 receptor antagonists also slightly inhibited the effect of quinpirole, their effects were significantly weaker than those of the D4 receptor antagonist. Furthermore, we showed that quinpirole selectively inhibits the CaV2.2 Ca2+ channels. Our results suggest that the activation of the D4 DA receptors is a promising strategy for pain management at the spinal cord level.

Neuroscience Letters published new progress about Analgesia. 21829-25-4 belongs to class pyridine-derivatives, name is Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, and the molecular formula is C17H18N2O6, Quality Control of 21829-25-4.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

den Hertog, H. J. published the artcileHetarynes. VI. Amination of bromoethoxypyridines, SDS of cas: 17117-13-4, the main research area is .

cf. CA 58, 11325a; 60, 1724d. Some bromoethoxypyridines were aminated with KNH2 in liquid NH3. The 3-bromo- and 4-bromoethoxypyridines reacted via hetaryne intermediates. The reaction of 2-bromo-6-ethoxypyridine proceeded via a rearrangement. 2-Bromo-4-ethoxypyridine, b2 104-6°, m. 35-6°, was prepared by treating 2-bromo-4-hydroxypyridine with diazoethane in Et2O for 16 hrs. at room temperature 4-Bromo-2-ethoxypyridine, m. 5.5-7°, was prepared from 4-amino-2-ethoxypyridine. Amination was carried out by adding 2.5 millimoles of the bromoethoxypyridine in Et2O to a solution prepared from 10 millimoles K and 30-40 ml. liquid NH3 in the presence of Fe(NO3)3 at -33° over a period of 10 min. (with stirring). The reaction-was stopped with 12 millimoles NH4Cl and the mixture evaporated, extracted with Et2O, and analyzed by gas chromatography. The following results were obtained [bromoethoxypyridine used and the aminoethoxypyridine(s) (molar ratio) produced given]: 4-bromo-2-ethoxy, 3-amino-2-ethoxy[-(1-2%)], 4-amino-2-ethoxy[-(98-99%)]; 4-bromo-3-ethoxy, 5-amino-3-ethoxy; 3-bromo-2-ethoxy, 3-amino-2-ethoxy (3), 4-amino-2-ethoxy (97); 3-bromo-4-ethoxy, 2-amino-4-ethoxy (55-60), 2-amino-5-bromo-4-ethoxy (15-20), 4-ethoxy (25); 3-bromo-5-ethoxy, 3-amino-5-ethoxy; 3-bromo-6-ethoxy, 3-amino-6-ethoxy (35), 4-amino-6-ethoxy (65); 2-bromo-3-ethoxy, 2-amino-3-ethoxy (99), 3-ethoxy (1); 2-bromo-4-ethoxy, 2-amino-4-ethoxy; 2-bromo-5-ethoxy, 2-amino-5-ethoxy (90-95), 5-ethoxy (5-10); 2-bromo-6-ethoxy, 2-amino-6-ethoxy (80-85), 4-amino-6-ethoxy (10-15).

Recueil des Travaux Chimiques des Pays-Bas published new progress about Amination. 17117-13-4 belongs to class pyridine-derivatives, name is 2-Bromo-4-ethoxypyridine, and the molecular formula is C7H8BrNO, SDS of cas: 17117-13-4.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem