Tag: M.W=300-350

Woolston, Esther published the artcileComparison of the effects on maternal endothelial cell activation: an in vitro study of anti-hypertensive drugs clinically used in pre-eclampsia, Formula: C17H18N2O6, the publication is Journal of Human Hypertension (2022), 36(2), 192-200, database is CAplus and MEDLINE.

Endothelial cell dysfunction in pregnancy, which can be induced by placental factors, is the fundamental component of the pathogenesis of pre-eclampsia. The dysfunctional vascular endothelium disrupts the balance of vasodilatory and vasoconstrictive factors, resulting in increasing blood pressure. There is currently no effective treatment for pre-eclampsia and effective control of hypertension may reduce neonatal morbidity and mortality by prolonging gestation, especially in cases of early onset disease. To date methyldopa, labetalol, nifedipine and metoprolol are recommended for controlling blood pressure in pre-eclampsia. All of these drugs have different mechanisms of action. In this in vitro study we investigated whether different types of anti-hypertensive drugs could have different effects on improving maternal endothelial cell dysfunction. Endothelial cells (HMEC-1) were exposed to phorbol-12-myristate-13-acetate (PMA) or pre-eclamptic sera or extracellular vesicles (EVs) derived from pre-eclamptic placentae, in the presence of each of the studied anti-hypertensive drugs (methyldopa, labetalol, nifedipine and metoprolol) or placebo for 24 h. Endothelial cell-surface adhesion mol. (ICAM-1) and monocyte adhesion were measured. The expression of cell-face ICAM-1 by HMEC-1 cells and THP-1 monocyte adherent to HMEC-1 that were exposed to three sep. well-known activators of endothelial cells in the presence of four anti-hypertensive drugs was significantly reduced regardless of the dose. However, the effect on the reduction of ICAM-1 expression and monocyte adhesion was not significantly different between the four medications. Our data suggest that the beneficial effect on improving endothelial cell function by these commonly prescribed anti-hypertensive drugs is seemingly independent of the anti-hypertensive mechanisms of the medication.

Journal of Human Hypertension 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 C14H10N2O, Formula: C17H18N2O6.

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

Palmquist, Karl H. published the artcileReciprocal cell-ECM dynamics generate supracellular fluidity underlying spontaneous follicle patterning, Recommanded Product: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the publication is Cell (Cambridge, MA, United States) (2022), 185(11), 1960-1973.e11, database is CAplus and MEDLINE.

During vertebrate embryogenesis, cell collectives engage in coordinated behavior to form tissue structures of increasing complexity. In the avian skin, assembly into follicles depends on intrinsic mech. forces of the dermis, but how cell mechanics initiate pattern formation is not known. Here, we reconstitute the initiation of follicle patterning ex vivo using only freshly dissociated avian dermal cells and collagen. We find that contractile cells phys. rearrange the extracellular matrix (ECM) and that ECM rearrangement further aligns cells. This exchange transforms a mech. unlinked collective of dermal cells into a continuum, with coherent, long-range order. Combining theory with experiment, we show that this ordered cell-ECM layer behaves as an active contractile fluid that spontaneously forms regular patterns. Our study illustrates a role for mesenchymal dynamics in generating cell-level ordering and tissue-level patterning through a fluid instability-processes that may be at play across morphol. symmetry-breaking contexts.

Cell (Cambridge, MA, 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 C17H18N2O6, Recommanded Product: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

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

Mimura, Kazuya published the artcileAtypical preeclampsia without underlying disease and elevated sFlt-1/ PlGF ratio, HPLC of Formula: 21829-25-4, the publication is Journal of Obstetrics and Gynaecology Research (2022), 48(2), 471-476, database is CAplus and MEDLINE.

Atypical preeclampsia before 20 wk of gestation without an underlying disease is very rare; however, the soluble Fms-like tyrosine kinase 1/placental growth factor (sFlt-1/PlGF) ratios remain unknown. Four pregnant women with no underlying disease, except for a history of childhood IgA vasculitis, developed preeclampsia at 13, 14, 17, and 18 wk of gestation with sFlt-1/PlGF ratios of 1589, 1183, 500, and 1460 pg/mL, resp. Their pregnancies were terminated, and they delivered within 2 wk. All previously abnormal clin. findings normalized within 3 mo. The sFlt-1/PlGF ratios were elevated in the four patients with atypical preeclampsia without underlying disease before 20 wk of gestation. A high sFlt-1/PlGF ratio may be indicative of preeclampsia when no underlying disease is present in pregnancies of less than 20 wk of gestation.

Journal of Obstetrics and Gynaecology Research 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, HPLC of Formula: 21829-25-4.

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

Tita, A. T. published the artcileTreatment for mild chronic hypertension during pregnancy, SDS of cas: 21829-25-4, the publication is New England Journal of Medicine (2022), 386(19), 1781-1792, database is CAplus and MEDLINE.

Background The benefits and safety of the treatment of mild chronic hypertension (blood pressure, <160/100 mm Hg) during pregnancy are uncertain. Data are needed on whether a strategy of targeting a blood pressure of less than 140/90 mm Hg reduces the incidence of adverse pregnancy outcomes without compromising fetal growth. methods In this open-label, multicenter, randomized trial, we assigned pregnant women with mild chronic hypertension and singleton fetuses at a gestational age of less than 23 wk to receive antihypertensive medications recommended for use in pregnancy (active-treatment group) or to receive no such treatment unless severe hypertension (systolic pressure, â‰?60 mm Hg; or diastolic pressure, â‰?05 mm Hg) developed (control group). The primary outcome was a composite of preeclampsia with severe features, medically indicated preterm birth at less than 35 wk’ gestation, placental abruption, or fetal or neonatal death. The safety outcome was small-for-gestational-age birth weight below the 10th percentile for gestational age. Secondary outcomes included composites of serious neonatal or maternal complications, preeclampsia, and preterm birth. results A total of 2408 women were enrolled in the trial. The incidence of a primary-outcome event was lower in the active-treatment group than in the control group (30.2% vs. 37.0%), for an adjusted risk ratio of 0.82 (95% confidence interval [CI], 0.74 to 0.92; P<0.001). The percentage of small-for-gestational-age birth weights below the 10th percentile was 11.2% in the active-treatment group and 10.4% in the control group (adjusted risk ratio, 1.04; 95% CI, 0.82 to 1.31; P = 0.76). The incidence of serious maternal complications was 2.1% and 2.8%, resp. (risk ratio, 0.75; 95% CI, 0.45 to 1.26), and the incidence of severe neonatal complications was 2.0% and 2.6% (risk ratio, 0.77; 95% CI, 0.45 to 1.30). The incidence of any preeclampsia in the two groups was 24.4% and 31.1%, resp. (risk ratio, 0.79; 95% CI, 0.69 to 0.89), and the incidence of preterm birth was 27.5% and 31.4% (risk ratio, 0.87; 95% CI, 0.77 to 0.99). conclusions In pregnant women with mild chronic hypertension, a strategy of targeting a blood pressure of less than 140/90 mm Hg was associated with better pregnancy outcomes than a strategy of reserving treatment only for severe hypertension, with no increase in the risk of small-for-gestational-age birth weight

New England Journal of Medicine 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 C6H8O3, SDS of cas: 21829-25-4.

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

Iwata, Naoko published the artcileClassification of pacemaker dynamics in the mouse intestine by field potential microimaging, HPLC of Formula: 21829-25-4, the publication is Biosensors and Bioelectronics: X (2022), 100111, database is CAplus.

The flexible and sophisticated movement of the gastrointestinal (GI) tract implies the involvement of mechanisms other than enteric neural circuits, to coordinate excitation in microregions. We thus performed microimaging of pacemaker dynamics in the small intestine of mice since it contains typical network-forming pacemaker cells. A dialysis membrane-reinforced low-impedance microelectrode array (MEA) enabled field potentials over a wide frequency range to be stably measured in microregions. The pacemaker dynamics were classified into basic patterns despite large variations. In the developmental process, pacemaker activity was categorized as either an ‘expanding’ or a ‘migrating’ pattern that was initiated in or propagated to the MEA sensing area, resp. The intercellular current of the volume conductor complicated the waveform of both activities. The existence of ‘expanding’ and ‘migrating’ patterns was attributable to duplicated pacemaker systems such as intracellular Ca2+ oscillation-activated and voltage-gated mechanisms. Addnl., from the spatio-temporal feature during the period of pacemaker events, the ‘bumpy/aberrant’ pattern was defined by aberrant, incoherent propagation, and associated with local impairment of excitability, while the ‘colliding/converging’ pattern involved the interaction of multiple activities in the MEA area. Interconversion between the four micro-coordination patterns occurred in the same microregion. 5-Hydroxytryptamine (5-HT) promoted ‘migrating’ activity, implying an improvement or restoration of spatial conductivity These results agree well with the action of 5-HT to change GI movement toward propulsion. In conclusion, our MEA method of microimaging classification enables the quant. assessment of spatio-temporal elec. coordination underlying GI motility, suggesting its application to small model animals.

Biosensors and Bioelectronics: X 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, HPLC of Formula: 21829-25-4.

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

Mendes, Ana Karla Bittencourt published the artcile1α,25-(OH)2 vitamin D3 prevents insulin resistance and regulates coordinated exocytosis and insulin secretion, Category: pyridine-derivatives, the publication is Journal of Nutritional Biochemistry (2022), 108864, database is CAplus and MEDLINE.

Vitamin D₃ is associated with improvements in insulin resistance and glycemia. In this study, we investigated the short-term effect of 1α,25-(OH)₂ Vitamin D₃ (1,25-D₃) and cholecalciferol (vitamin D₃) on the glycemia and insulin sensitivity of control and dexamethasone-induced insulin-resistance rats. ⁴⁵Ca²⁺ influx responses to 1,25-D₃ and its role in insulin secretion were investigated in isolated pancreatic islets from control rats. In vivo, 5 d treatment with 1,25-D₃ (i.p.) prevented insulin resistance in dexamethasone-treated rats. Treatment with 1,25-D₃ improved the activities of hepatic enzymes, serum lipids and calcium concentrations in insulin-resistant rats. 25-D₃ (o.g.) does not affect insulin resistance. In pancreatic islets, 1,25-D₃ increased insulin secretion and stimulated rapid response ⁴⁵Ca²⁺ influx. The stimulatory effect of 1,25-D₃ on ⁴⁵Ca²⁺ influx was decreased by diazoxide, apamine, thapsigargin, dantrolene, 2-APB, nifedipine, TEA, PKA, PKC, and cytoskeleton inhibitor, while it was increased by glibenclamide and N-ethylmaleimide. The stimulatory effect of 1,25-D₃ on ⁴⁵Ca²⁺ influx involves the activation of L-type VDCC, K⁺-ATP, K⁺-Ca²⁺, and Kv channels, which augment cytosolic calcium. These ionic changes mobilize calcium from stores and downstream activation of PKC, PKA tethering vesicle traffic and fusion at the plasma membrane for insulin secretion. This is the first study highlighting the unprecedented role of 1,25-D₃ (short-term effect) in the regulation of glucose homeostasis and on prevention of insulin resistance. Furthermore, this study shows the intracellular β-cell signal transduction of 1,25-D₃ through the modulation of pivotal ionic channels and proteins exhibiting a coordinated exocytosis of vesicles for insulin secretion.

Journal of Nutritional Biochemistry 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, Category: pyridine-derivatives.

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

Vaibavi, S. R. published the artcileCalcium-channel-blockers exhibit divergent regulation of cancer extravasation through the mechanical properties of cancer cells and underlying vascular endothelial cells, Computed Properties of 21829-25-4, the publication is Cell Biochemistry and Biophysics (2022), 80(1), 171-190, database is CAplus and MEDLINE.

Cardiovascular and cancer illnesses often co-exist, share pathol. pathways, and complicate therapy. In the context of the potential oncol. role of cardiovascular-antihypertensive drugs (AHD), here we examine the role of calcium-channel blocking drugs on mechanics of extravasating cancer cells, choosing two clin.-approved calcium-channel blockers (CCB): Verapamil-hydrochloride and Nifedipine, as model AHD to simultaneously target cancer cells (MCF7 and or MDA231) and an underlying monolayer of endothelial cells (HUVEC). First, live-cell microscopy shows that exposure to Nifedipine increases the spreading-area, migration-distance, and frequency of transmigration of MCF-7 cells through the HUVEC monolayer, whereas Verapamil has the opposite effect. Next, impedance-spectroscopy shows that for monolayers of either endothelial or cancer cells, Nifedipine-treatment alone decreases the impedance of both cases, suggesting compromised cell-cell integrity. Furthermore, upon co-culturing MCF-7 on the HUVEC monolayers, Nifedipine-treated MCF-7 cells exhibit weaker impedance than Verapamil-treated MCF-7 cells. Following, fluorescent staining of CCB-treated cytoskeleton, focal adhesions, and cell-cell junction also indicated that Nifedipine treatment diminished the cell-cell integrity, whereas verapamil treatment preserved the integrity. Since CCBs regulate intracellular Ca2+, we next investigated if cancer cell′s exposure to CCBs regulates calcium-dependent processes critical to extravasation, specifically traction and mechanics of plasma membrane. Towards this end, first, we quantified the 2D-cellular traction of cells in response to CCBs. Results show that exposure to F-actin depolymerizing drug decreases traction stress significantly only for Nifedipine-treated cells, suggesting an actin-independent mechanism of Verapamil activity. Next, using an optical tweezer to quantify the mechanics of plasma membrane (PM), we observe that under constant, externally-applied tensile strain, PM of Nifedipine-treated cells exhibits smaller relaxation-time than Verapamil and untreated cells. Finally, actin depolymerization significantly decreases MSD only for Verapamil treated cancer-cells and endothelial cells and not for Nifedipine-treated cells. Together, our results show that CCBs can have varied, mechanics-regulating effects on cancer-cell transmigration across endothelial monolayers. A judicious choice of CCBs is critical to minimizing the pro-metastatic effects of antihypertension therapy.

Cell Biochemistry and Biophysics 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 C5H7BO2S, Computed Properties of 21829-25-4.

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

Pickles, G. M. published the artcileThe reactions of diborane with aryl organotin compounds, Application of Triphenyl(pyridin-1-ium-1-yl)borate, the publication is Journal of Organometallic Chemistry (1984), 260(1), 7-15, database is CAplus.

Treating R₄Sn (R = Ph, 2- and 4-tolyl, 4-ClC₆H₄) and Ph₃SnX (X = Cl, H, OH, OAc, O₂CCF₃) with BH₃ gave transmetalation, in which â‰? aryl group was transferred to B. The organoboron intermediates give phenols upon oxidation and boronic and borinic acids upon hydrolysis. Pyridine (L) complexes of organoboranes, Ph₂BHL and Ph₃BL were also isolated.

Journal of Organometallic 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 C23H20BN, Application of Triphenyl(pyridin-1-ium-1-yl)borate.

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

Trezza, Alfonso published the artcileFunctional, electrophysiology, and molecular dynamics analysis of quercetin-induced contraction of rat vascular musculature, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the publication is European Journal of Pharmacology (2022), 174778, database is CAplus and MEDLINE.

Quercetin, a flavonoid abundantly present in the Mediterranean diet, is considered a vasodilator despite its recognized capability to stimulate vascular CaV1.2 channel current (ICa1.2). The present study was undertaken to assess its possible vasocontractile activity. Functional and electrophysiol. experiments were performed in vitro on rat aorta rings and tail artery myocytes along with an in-depth mol. modeling anal. The CaV1.2 channel stimulator (S)-(-)-methyl-1,4-dihydro-2,6-dimethyl-3-nitro-4-(2-trifluoromethylphenyl) pyridine-5-carboxylate (Bay K 8644) was used as reference compound Quercetin and Bay K 8644 caused a significant leftward shift of KCl concentration-response curve. Neither agent affected basal muscle tone, though in rings pre-treated with thapsigargin or 15 mM KCl they caused a strong, concentration-dependent contraction. Both quercetin and Bay K 8644 potentiated the response to Ca²⁺ in weakly depolarised rings. At high KCl concentrations, however, quercetin caused vasorelaxation. While Bay K 8644 stimulated ICa1.2, this effect being sustained with time, quercetin-induced stimulation was transient, although the mol. in solution underwent only marginal oxidation Quercetin transient stimulation was not affected by pre-treatment with isoprenaline, sodium nitroprusside, or dephostatin; however, it converted to a sustained one in myocytes pre-incubated with Go6976. Classical mol. dynamics simulations revealed that quercetin and Bay K 8644 formed hydrogen bonds with target sensing residues of CaV1.2 channel favoring the inactivated conformation. In conclusion, quercetin-induced stimulation of ICa1.2 promoted vasocontraction when Ca²⁺ buffering function of sarcoplasmic reticulum was impaired and/or smooth muscle cell membrane was moderately depolarised, as it may occur under certain pathol. conditions.

European Journal of Pharmacology 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 C18H28N2O7, 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

Gohil, Vishal M. published the artcileNutrient-sensitized screening for drugs that shift energy metabolism from mitochondrial respiration to glycolysis, Recommanded Product: N-Methyl-2-(pyridin-2-yl)ethan-1-amine dimethanesulfonate, the publication is Nature Biotechnology (2010), 28(3), 249-255, database is CAplus and MEDLINE.

Most cells have the inherent capacity to shift their reliance on glycolysis relative to oxidative metabolism, and studies in model systems have shown that targeting such shifts may be useful in treating or preventing a variety of diseases ranging from cancer to ischemic injury. However, we currently have a limited number of mechanistically distinct classes of drugs that alter the relative activities of these two pathways. We screen for such compounds by scoring the ability of >3500 small mols. to selectively impair growth and viability of human fibroblasts in media containing either galactose or glucose as the sole sugar source. We identify several clin. used drugs never linked to energy metabolism, including the antiemetic meclizine, which attenuates mitochondrial respiration through a mechanism distinct from that of canonical inhibitors. We further show that meclizine pretreatment confers cardioprotection and neuroprotection against ischemia-reperfusion injury in murine models. Nutrient-sensitized screening may provide a useful framework for understanding gene function and drug action within the context of energy metabolism

Nature Biotechnology 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, Recommanded Product: N-Methyl-2-(pyridin-2-yl)ethan-1-amine dimethanesulfonate.

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