Tag: M.W=200-350

Han, Jung Woo published the artcileIsoproterenol-induced hypertrophy of neonatal cardiac myocytes and H9c2 cell is dependent on TRPC3-regulated CaV1.2 expression, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is TRPC3 calcium channel signaling cardiac myocyte hypertrophy; Ca(2+) influx; Ca(V)1.2; L-type Ca(2+) channel; NFAT3; Neonatal cardiac hypertrophy; Transient receptor potential canonical channel 3.

CaV1.2 and transient receptor potential canonical channel 3 (TRPC3) are two proteins known to have important roles in pathol. cardiac hypertrophy; however, such roles still remain unclear. A better understanding of these roles is important for furthering the clin. understanding of heart failure. We previously reported that Trpc3-knockout (KO) mice are resistant to pathol. hypertrophy and that their CaV1.2 protein expression is reduced. In this study, we aimed to examine the relationship between these two proteins and characterize their role in neonatal cardiomyocytes. We measured CaV1.2 expression in the hearts of wild-type (WT) and Trpc3-/- mice, and examined the effects of Trpc3 knockdown and overexpression in the rat cell line H9c2. We also compared the hypertrophic responses of neonatal cardiomyocytes cultured from Trpc3-/- mice to a representative hypertrophy-causing drug, isoproterenol (ISO), and measured the activity of nuclear factor of activated T cells 3 (NFAT3) in neonatal cardiomyocytes (NCMCs). We inhibited the L-type current with nifedipine, and measured the intracellular calcium concentration using Fura-2 with 1-oleoyl-2-acetyl-sn-glycerol (OAG)-induced Ba2+ influx. When using the Trpc3-mediated Ca2+ influx, both intracellular calcium concentration and calcium influx were reduced in Trpc3-KO myocytes. Not only was the expression of CaV1.2 greatly reduced in Trpc3-KO cardiac lysate, but the size of the CaV1.2 currents in NCMCs was also greatly reduced. When NCMCs were treated with Trpc3 siRNA, it was confirmed that the expression of CaV1.2 and the intracellular nuclear transfer activity of NFAT decreased. In H9c2 cells, the ISO activated- and verapamil inhibited- Ca2+ influxes were dramatically attenuated by Trpc3 siRNA treatment. In addition, it was confirmed that both the expression of CaV1.2 and the size of H9c2 cells were regulated according to the expression and activation level of TRPC3. We found that after stimulation with ISO, cell hypertrophy occurred in WT myocytes, while the increase in size of Trpc3-KO myocytes was greatly reduced. These results suggest that not only the cell hypertrophy process in neonatal cardiac myocytes and H9c2 cells were regulated according to the expression level of CaV1.2, but also that the expression level of CaV1.2 was regulated by TRPC3 through the activation of NFAT.

Cell Calcium published new progress about Cardiac hypertrophy. 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, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Inan, Cihan published the artcileComparison of the efficacy of the immediate-release and osmotic push-pull system formulations of nifedipine for tocolysis, HPLC of Formula: 21829-25-4, the main research area is hemorrhage respiratory distress syndrome enterocolitis; neonate; nifedipine; preterm labor; tocolysis; uterine contraction.

To compare the immediate-release (IR) and osmotic push-pull system formulations of nifedipine used for tocolysis in prolonging pregnancy, neonatal outcomes and maternal-fetal adverse effects. We evaluated 140 pregnant women who received the IR (n = 72) and osmotic push-pull system (n = 68) formulations of nifedipine for tocolysis due to threatened preterm labor between 240/7 and 336/7 wk of gestation. Groups were compared in terms of efficacy of tocolysis in prolonging pregnancy for more than 48 h, 7 days and up to 37 wk of gestation, total number of days gained for prolonging pregnancy, delivery weeks, maternal-fetal adverse effects and neonatal outcomes including ventilation support, need for intubation or surfactant, intraventricular hemorrhage, respiratory distress syndrome, necrotizing enterocolitis, admission to neonatal intensive care unit, neonatal death, Apgar scores at the 1st and 5th minutes. There was no significant difference between the two groups in prolonging pregnancy for more than 48 h or 7 days, total number of days gained after tocolysis initiation, delivery weeks, the number of births at 340/7-366/7 wk or after 37 wk of gestation (P > 0.05). Maternal-fetal adverse effects and neonatal outcomes were similar in both groups (P > 0.05). The efficacy of IR and osmotic push-pull system formulations of nifedipine have similar effects in terms of tocolysis and neonatal outcomes, adverse effects. Osmotic push-pull system formulation of nifedipine may be an alternative medication in tocolytic therapy due to its ease of use and the absence of loading dose necessity.

Journal of Obstetrics and Gynaecology Research published new progress about Cervical dilatation. 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, HPLC of Formula: 21829-25-4.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Lee, Chin-Mei published the artcileGIGANTEA recruits the UBP12 and UBP13 deubiquitylases to regulate accumulation of the ZTL photoreceptor complex, Category: pyridine-derivatives, the main research area is Arabidopsis seed UBP12 UBP13 GIGANTEA ZTL photoreceptor complex.

ZEITLUPE (ZTL), a photoreceptor with E3 ubiquitin ligase activity, communicates end-of-day light conditions to the plant circadian clock. It still remains unclear how ZTL protein accumulates in the light but does not destabilize target proteins before dusk. Two deubiquitylating enzymes, UBIQUITIN-SPECIFIC PROTEASE 12 and 13 (UBP12 and UBP13), which regulate clock period and protein ubiquitylation in a manner opposite to ZTL, associate with the ZTL protein complex. Here we demonstrate that the ZTL interacting partner, GIGANTEA (GI), recruits UBP12 and UBP13 to the ZTL photoreceptor complex. We show that loss of UBP12 and UBP13 reduces ZTL and GI protein levels through a post-transcriptional mechanism. Furthermore, a ZTL target protein is unable to accumulate to normal levels in ubp mutants. This demonstrates that the ZTL photoreceptor complex contains both ubiquitin-conjugating and -deconjugating enzymes, and that these two opposing enzyme types are necessary for circadian clock pacing. This shows that deubiquitylating enzymes are a core element of circadian clocks, conserved from plants to animals.

Nature Communications published new progress about Arabidopsis thaliana. 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, Category: pyridine-derivatives.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Limanjaya, Ivan published the artcileL-selectin activation regulates Rho GTPase activity via Ca+2 influx in Sertoli cell line, ASC-17D cells, Product Details of C17H18N2O6, the main research area is L selectin Rho GTPase calcium channel sertoli cell; ASC-17D cells; Calcium influx; L-selectin; Rho GTPase.

In seminiferous epithelium, tight junctions (TJs) between adjacent Sertoli cells constitute the blood-testis barrier and must change synchronically for germ cells to translocate from the basal to the adluminal compartment during the spermatogenic cycle. Rho GTPase activation through stimulation with specific L-selectin ligands has been proposed to modulate tight junctional dynamics. However, little is known regarding the role of Ca+2 dynamics in Sertoli cell and how Ca+2 relays L-selectin signals to modulate Rho GTPase activity in Sertoli cells, thus prompting us to investigate the Ca+2 flux induced by L-selectin ligand in ASC-17D cells. Using fluorescent real-time image, we first demonstrated the increase of intracellular Ca+2 level following L-selectin ligand stimulation. This Ca+2 increase was inhibited in ASC-17D cells pretreated with nifedipine, the L-type voltage-operated Ca+2 channel (VOCC) blocker, but not mibefradil, the T-type VOCC blocker. We then demonstrated the up-regulation of Rho and Rac1 in ASC-17D cells following the administration of L-selectin ligand, and the pre-treatment with nifedipine, but not mibefradil, prior to L-selectin ligand-binding abolished the activation of both Rho and Rac1. Together, we conclude that the activation of L-selectin induces Ca+2 influx through the L-type VOCC, which up-regulates Rho and Rac1 proteins, in ASC-17D cells.

Biochemical and Biophysical Research Communications published new progress about Blood-testis barrier. 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, Product Details of C17H18N2O6.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Cheng, Sixue published the artcileNanoconfinement Effects on the Glass Transition and Crystallization Behaviors of Nifedipine, Synthetic Route of 21829-25-4, the main research area is glass transition crystallization nifedipine; amorphous pharmaceutical; cold-crystallization; glass transition; nifedipine; polymorphism.

The impact of nanoconfinement on the crystallization and glass transition behaviors of nifedipine (NIF) has been investigated using differential scanning calorimetry. Nanoconfinement was provided by imbibing the NIF into a porous medium (controlled pore glass, CPG), and results were compared with the unconfined bulk material. Consistent with previous results from the literature, both glass transition temperature Tg and melting temperature Tm decrease with decreasing pore size. The melting temperature was found to decrease with the reciprocal of pore diameter and could be analyzed with the Gibbs-Thomson equation. In addition, for confinement sizes of 7.5 and 12 nm, it was found that no cold-crystallization occurs upon heating from the glassy state to above the expected melting transition. Finally, at intermediate confinements we find evidence of a possible new, confinement-induced polymorph of NIF.

Molecular Pharmaceutics published new progress about Crystal polymorphism. 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, Synthetic Route of 21829-25-4.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Tsai, Yuan-Ming published the artcileVascular Kv7 channels control intracellular Ca2+ dynamics in smooth muscle, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is retigabine vasopressin calcium phospholipase smooth muscle; Calcium; Kv7; Phospholipase C; Retigabine; T-type Ca(2+)channels; Vascular smooth muscle cell; Vasopressin.

Voltage-gated Kv7 (or KCNQ) channels control activity of excitable cells, including vascular smooth muscle cells (VSMCs), by setting their resting membrane potential and controlling other excitability parameters. Excitation-contraction coupling in muscle cells is mediated by Ca2+ but until now, the exact role of Kv7 channels in cytosolic Ca2+ dynamics in VSMCs has not been fully elucidated. We utilized microfluorimetry to investigate the impact of Kv7 channel activity on intracellular Ca2+ levels and elec. activity of rat A7r5 VSMCs and primary human internal mammary artery (IMA) SMCs. Both, direct (XE991) and G protein coupled receptor mediated (vasopressin, AVP) Kv7 channel inhibition induced robust Ca2+ oscillations, which were significantly reduced in the presence of Kv7 channel activator, retigabine, L-type Ca2+ channel inhibitor, nifedipine, or T-type Ca2+ channel inhibitor, NNC 55-0396, in A7r5 cells. Membrane potential measured using FluoVolt exhibited a slow depolarisation followed by a burst of sharp spikes in response to XE991; spikes were temporally correlated with Ca2+ oscillations. Phospholipase C inhibitor (edelfosine) reduced AVP-induced, but not XE991-induced Ca2+ oscillations. AVP and XE991 induced a large increase of [Ca2+]i in human IMA, which was also attenuated with retigabine, nifedipine and NNC 55-0396. RT-PCR, immunohistochem. and electrophysiol. suggested that Kv7.5 was the predominant Kv7 subunit in both rat and human arterial SMCs; CACNA1C (Cav1.2; L-type) and CACNA1 G (Cav3.1; T-type) were the most abundant voltage-gated Ca2+ channel gene transcripts in both types of VSMCs. This study establishes Kv7 channels as key regulators of Ca2+ signalling in VSMCs with Kv7.5 playing a dominant role.

Cell Calcium published new progress about Immunohistochemistry. 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

Lee, Chien-Chang published the artcileUse of calcium channel blockers and risk of active tuberculosis disease a population-based analysis, Recommanded Product: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is calcium channel blocker tuberculosis disease human; calcium channel blockers; heart failure; hypertension; pharmacoepidemiology; tuberculosis.

Calcium channel blockers (CCBs) are known to reduce the availability of iron-an important mineral for intracellular pathogens. Nonetheless, whether the use of CCBs modifies the risk of active tuberculosis in the clin. setting remains unclear. To determine whether CCBs may modify the risk of active tuberculosis disease, we conducted a nested case-control study using the National Health Insurance Research Database of Taiwan between Jan. 1999 and Dec. 2011. Conditional logistic regression and disease risk score adjustment were used to calculate the risk of active tuberculosis disease associated with CCB use. Subgroup anal. investigated the effect of different types of CCBs and potential effect modification in different subpopulations. A total of 8164 new active tuberculosis cases and 816 400 controls were examined Use of CCBs was associated with a 32% decrease in the risk of active tuberculosis (relative risk [RR], 0.68 [95% CI, 0.58-0.78]) after adjustment with disease risk score. Compared with nonuse of CCBs, the use of dihydropyridine CCBs was associated with a lower risk of tuberculosis (RR, 0.63 [95% CI, 0.53-0.79]) than nondihydropyridine CCBs (RR, 0.73 [95% CI, 0.57-0.94]). In contrast, use of β-blockers (RR, 0.99 [95% CI, 0.83-1.12]) or loop diuretics (RR, 0.88 [95% CI, 0.62-1.26]) was not associated with lower risk of tuberculosis. In subgroup anal., the risk of tuberculosis associated with the use of CCBs was similar among patients with heart failure or cerebrovascular diseases. Our study confirms that use of dihydropyridine CCBs decreases the risk of active tuberculosis.

Hypertension published new progress about Acute heart failure. 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, Recommanded Product: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Suzuki, Hiroyuki published the artcileAcute kidney injury successfully treated with autologous granulocyte colony-stimulating factor-mobilized peripheral blood CD34 -positive cell transplantation: A first-in-human report, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is autologous GCSF peripheral blood cell transplantation acute kidney injury; CD34+; clinical trials; granulocyte-colony stimulating factor (G-CSF); hematopoietic stem cells (HSCs); kidney; stem cell transplantation.

A 36-yr-old man with severe acute kidney injury (AKI) was admitted to Shonan Kamakura General Hospital in Japan. He was diagnosed with refractory hypertension based on a severely elevated blood pressure of 224/116 mmHg and retinal, cardiac, and brain damage revealed by ECG, fundoscopy, and magnetic resonance imaging, resp. Although hemodialysis was withdrawn following strict blood pressure control by an angiotensin receptor blocker, severe kidney insufficiency persisted. Therefore, we performed an autologous granulocyte colonystimulating factor-mobilized peripheral blood CD34-pos. cell transplantation. Collected CD34-pos. cells were directly infused to both renal arteries. The patient’s general condition was unremarkable after intervention, and the serum creatinine level gradually improved to 2.96 mg/dL 23 wk after cell therapy. Although transient fever and thrombocytosis were observed after intervention, no major adverse events were observed This patient is the first case in a phase I/II clin. trial of autologous granulocyte colony-stimulating factor-mobilized peripheral blood CD34-pos. cell transplantation for severe AKI with a CD34-pos. cell doseescalating protocol (trial number jRCTb030190231).

Stem Cells Translational Medicine published new progress about Acute kidney injury. 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, Name: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Morgan, John A. published the artcileChronic hypertension in pregnancy: are outcomes the same in patients on antihypertensives?*, Recommanded Product: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is antihypertensive chronic hypertension pregnancy maternal outcomes; Antihypertensives; chronic hypertension; maternal outcomes; neonatal outcomes; pregnancy.

To investigate differences in maternal and fetal outcomes among pregnant patients with chronic hypertension requiring antihypertensives for adequate control vs. those who do not require antihypertensives. Single-site retrospective cohort study including pregnant patients with chronic hypertension from 2015-2018. Two groups included those who required antihypertensives vs. those who did not. Primary outcome is composite morbidity: pregnancy loss after 20 wk, IUGR, maternal death, maternal stroke or TIA, pulmonary edema, renal failure, hypertensive emergency, HELLP syndrome, placental abruption or delivery before 34 wk. Secondary outcomes included development of severe features, indication for preterm labor less than 37 wk, incidence of severe range blood pressures, and neonatal outcomes. Student t, chi square, and Kruskal-Wallis tests where appropriate. Logistic regression used to account for potential confounders. Study cohort included 117 on antihypertensives and 114 not on antihypertensives. Use of antihypertensives was associated with the composite primary outcome (Odds ratio [OR], 3.88; 95% confidence interval [CI], 1.66-9.78). Use of antihypertensive medications was also associated with increased risk of prenatal diagnosis of IUGR, delivery prior to 34 wk, development of severe features, severe blood pressure during pregnancy, earlier mean gestational age at delivery, lower mean birth weight, and higher risk of NICU admission. Logistic regression anal. showed that the association between medication requirement and our composite primary outcome persisted even after adjustment for age, BMI, and presence of gestational diabetes. Our findings show an association between the requirement of antihypertensive medication use a significantly higher risk of composite primary outcome, prenatal diagnosis of IUGR, delivery prior to 34 wk, and the development of severe features.

Journal of Maternal-Fetal & Neonatal Medicine published new progress about Acute renal failure. 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, Recommanded Product: Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Sarabu, Sandeep published the artcileHypromellose acetate succinate based amorphous solid dispersions via hot melt extrusion: Effect of drug physicochemical properties, Formula: C17H18N2O6, the main research area is hypromellose acetate succinate amorphous solid dispersion hot melt extrusion; Efavirenz; HME; HPMCAS; Nifedipine; Solid dispersions; Supersaturation.

In this study, the impact of drug and hydroxypropyl methylcellulose acetate succinate (HPMCAS) grades physicochem. properties on extrusion process, dissolution and stability of the hot melt extruded amorphous solid dispersions (ASDs) of nifedipine and efavirenz was investigated. Incorporation of drugs affected the extrusion temperature required for solid dispersion preparation Differential scanning calorimetry and powder X-ray diffraction studies confirmed the amorphous conversion of the drugs in the prepared formulations. The amorphous nature of ASDs was unchanged after 3 mo of stability testing at 40°C and 75% relative humidity. The dissolution efficiency of the ASDs was dependent on the log P of the drug. The inhibitory effect of HPMCAS on drug precipitation was dependent on the hydrophobic interactions between drug and polymer, polymer grade, and dose of the drug. The dissolution efficiency and dissolution rate of the ASDs were dependent on the log P of the drug and solubility and hydrophilicity of the polymer grade resp. The inhibitory effect of HPMCAS on drug precipitation was dependent on the hydrophobic interactions between drug and polymer, polymer grade, and the dissolution dose of the drug.

Carbohydrate Polymers published new progress about Amorphous materials. 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, Formula: C17H18N2O6.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem