Category: 21829-25-4

Rivera-Gonzalez, Jonatahan published the artcileUse of Sublingual Nitrates for Management of Limb Ischemia Secondary to Inadvertent Intra-Arterial Buprenorphine/Naloxone (Suboxone®) Film Injection., Related Products of pyridine-derivatives, the main research area is Buprenorphine; Intravenous drug user; Limb ischemia; Naloxone; Nitroglycerine; Suboxone.

Multiple case reports have signaled a rise in buprenorphine abuse in the US, particularly among inmates. We present the case of limb ischemia secondary to accidental intra-arterial buprenorphine/naloxone film injection successfully treated with sublingual nitroglycerin. A 39-year-old man with history of intravenous drug use presented sudden severe left hand pain since three days prior to evaluation. Pain was preceded by self-injection of dissolved buprenorphine/naloxone sublingual film onto the affected arm. An arteriogram suggested severe vasoconstriction in the absence of frank thrombosis. Patient was initially treated with continuous heparin infusion and nifedipine. Forty-eight hours later, due to poor response, sublingual nitroglycerin was added to therapy. Digits regained color, sensation, and pain resolved within 15 minutes of administration of sublingual nitroglycerin. The presence of acute limb ischemia caused by prolonged vasospasm is a very rare complication. A normal angiogram should raise suspicion regarding vasospasm as the mechanism of ischemia, and prompt nitroglycerin therapy.

Puerto Rico health sciences journal published new progress about Buprenorphine; Intravenous drug user; Limb ischemia; Naloxone; Nitroglycerine; Suboxone. 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

Suzuki, Yoshiaki published the artcileLocal Ca2+ Signals within Caveolae Cause Nuclear Translocation of CaMK1α in Mouse Vascular Smooth Muscle Cells., SDS of cas: 21829-25-4, the main research area is Ca2+/calmodulin-dependent kinase; L-type Ca2+ channel; caveola; fluorescence imaging; vascular smooth muscle cell.

An increase in intracellular Ca2+ concentration ([Ca2+]i) activates Ca2+-sensitive enzymes such as Ca2+/calmodulin-dependent kinases (CaMK) and induces gene transcription in various types of cells. This signaling pathway is called excitation-transcription (E-T) coupling. Recently, we have revealed that a L-type Ca2+ channel/CaMK kinase (CaMKK) 2/CaMK1α complex located within caveolae in vascular smooth muscle cells (SMCs) can convert [Ca2+]i changes to gene transcription profiles that are related to chemotaxis. Although CaMK1α is expected to be the key molecular identity that can transport Ca2+ signals originated within caveolae to the nucleus, data sets directly proving this scheme are lacking. In this study, multicolor fluorescence imaging methods were utilized to address this question. Live cell imaging using mouse primary aortic SMCs revealed that CaMK1α can translocate from the cytosol to the nucleus; and that this movement was blocked by nifedipine or a CaMKK inhibitor, STO609. Experiments using two types of Ca2+ chelators, ethylene glycol-bis(2-aminoethylether)-N,N,N’,N’-tetraacetic acid (EGTA) and 1,2-bis(2-aminophenoxy)ethane-N,N,N’,N’-tetraacetic acid (BAPTA), combined with caveolin-1 knockout (cav1-KO) mice showed that local Ca2+ events within caveolae are required to trigger this CaMK1α nuclear translocation. Importantly, overexpression of cav1 in isolated cav1-KO myocytes recovered the CaMK1α translocation. In SMCs freshly isolated from mesenteric arteries, CaMK1α was localized mainly within caveolae in the resting state. Membrane depolarization induced both nuclear translocation and phosphorylation of CaMK1α. These responses were inhibited by nifedipine, STO609, cav1-KO, or BAPTA. These new findings strongly suggest that CaMK1α can transduce Ca2+ signaling generated within or very near caveolae to the nucleus and thus, promote E-T coupling.

Biological & pharmaceutical bulletin published new progress about Ca2+/calmodulin-dependent kinase; L-type Ca2+ channel; caveola; fluorescence imaging; vascular smooth muscle cell. 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

Reddy, Suryanarayana Challa published the artcileAmlodipine Induced Gum Hypertrophy: A Rare Case Report., Product Details of C17H18N2O6, the main research area is Calcium channel blockers; amlodipine; anticonvulsants; antihypertensive; drug induced gingival overgrowth; immunosuppressive.

BACKGROUND: DIGO or drug-induced gingival overgrowth occurs as a side effect of certain drugs. Until now, the etiology of drug-induced gingival overgrowth is not clearly understood. Among the calcium channel blockers, nifedipine has been shown to be most frequently associated with drug-induced gingival hyperplasia. Amlodipine is a comparatively newer calcium channel blocker that with a longer duration of action and lesser side effects as compared to nifedipine. There are only certain case reports of amlodipine-induced gum hyperplasia. CASE PRESENTATION: We report a case of amlodipine-induced gum hyperplasia in a 66-year-old hypertensive patient taking amlodipine at a dose of 5 mg once a day. There was significant regression of gum hypertrophy after substitution of amlodipine by Losartan. CONCLUSION: Amlodipine is one of the commonly prescribed antihypertensive drugs, and gingival hyperplasia is one overlooked side effect in patients taking amlodipine. Awareness of this potential side effect of amlodipine may be helpful to reduce the anxiety of patients and the cost of diagnostic procedures.

Current drug safety published new progress about Calcium channel blockers; amlodipine; anticonvulsants; antihypertensive; drug induced gingival overgrowth; immunosuppressive. 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

Milliner, Brendan H A published the artcileEffect of Calcium-Channel Blockade on the Cold-Induced Vasodilation Response., Computed Properties of 21829-25-4, the main research area is calcium channel blockers; cold injury; environmental medicine; prevention and control.

INTRODUCTION: Cold-induced vasodilation (CIVD) is seen in the extremities during exposure to cold. A strong vasodilation response has been associated with a decreased risk of cold injury. Increasing CIVD might further decrease this risk. The calcium-channel blocker nifedipine causes vasodilation and is used to treat Raynaud’s syndrome and chilblains. Nifedipine is also used for high altitude pulmonary edema and could potentially serve a dual purpose in preventing frostbite. The effects of nifedipine on CIVD have not been studied. METHODS: A double-blind crossover study comparing nifedipine (30 mg SR (sustained release) orally twice daily) to placebo was designed using 2 sessions of 4 finger immersion in 5°C water, with 24 h of medication pretreatment before each session. Finger temperatures were measured via nailbed thermocouples. The primary outcome was mean finger temperature; secondary outcomes were mean apex and nadir temperatures, first apex and nadir temperatures, subjective pain ranking, and time of vasodilation onset (all presented as mean±SD). RESULTS: Twelve volunteers (age 29±3 [24-34] y) completed the study. No significant difference in finger temperature (9.2±1.1°C nifedipine vs 9.0±0.7°C placebo, P=0.38) or any secondary outcome was found. Pain levels were similar (2.8±1.6 nifedipine vs 3.0±1.5 placebo, P=0.32). The most common adverse event was headache (32% of nifedipine trials vs 8% placebo). CONCLUSIONS: Pretreatment with 30 mg of oral nifedipine twice daily does not affect the CIVD response in healthy individuals under cold stress.

Wilderness & environmental medicine published new progress about calcium channel blockers; cold injury; environmental medicine; prevention and control. 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

Hoffmann, Tal published the artcilePainful diabetic neuropathy leads to functional Cav3.2 expression and spontaneous activity in skin nociceptors of mice, Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is painful diabetic neuropathy CaV expression spontaneous activity skin nociceptor; Calcitonin gene-related peptide; Excitability; Neuropathic pain; Neuropeptide release; Sciatic nerve; T-type calcium channel; TTA-P2.

Painful diabetic neuropathy occurs in approx. 20% of diabetic patients with underlying pathomechanisms not fully understood. We evaluated the contribution of the Cav3.2 isoform of T-type calcium channel to hyperglycemia-induced changes in cutaneous sensory C-fiber functions and neuropeptide release employing the streptozotocin (STZ) diabetes model in congenic mouse strains including global knockouts (KOs). Hyperglycemia established for 3-5 wk in male C57BL/6J mice led to major reorganizations in peripheral C-fiber functions. Unbiased electrophysiol. screening of mechanosensitive single-fibers in isolated hairy hindpaw skin revealed a relative loss of (polymodal) heat sensing in favor of cold sensing. In healthy Cav3.2 KO mice both heat and cold sensitivity among the C-fibers seemed underrepresented in favor of exclusive mechanosensitivity, low-threshold in particular, which deficit became significant in the diabetic KOs. Diabetes also led to a marked increase in the incidence of spontaneous discharge activity among the C-fibers of wildtype mice, which was reduced by the specific Cav3.2 blocker TTA-P2 and largely absent in the KOs. Evaluation restricted to the peptidergic class of nerve fibers – measuring KCl-stimulated CGRP release – revealed a marked reduction in the sciatic nerve by TTA-P2 in healthy but not diabetic wildtypes, the latter showing CGRP release that was as much reduced as in healthy and, to the same extent, in diabetic Cav3.2 KOs. These data suggest that diabetes abrogates all Cav3.2 functionality in the peripheral nerve axons. In striking contrast, diabetes markedly increased the KCl-stimulated CGRP release from isolated hairy skin of wildtypes but not KO mice, and TTA-P2 reversed this increase, strongly suggesting a de novo expression of Cav3.2 in peptidergic cutaneous nerve endings which may contribute to the enhanced spontaneous activity. De-glycosylation by neuraminidase showed clear desensitizing effects, both in regard to spontaneous activity and stimulated CGRP release, but included actions independent of Cav3.2. However, as diabetes-enhanced glycosylation is decisive for intra-axonal trafficking, it may account for the substantial reorganizations of the Cav3.2 distribution. The results may strengthen the validation of Cav3.2 channel as a therapeutic target of treating painful diabetic neuropathy.

Experimental Neurology published new progress about Axon. 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

Hollingworth, Samantha A. published the artcileAntihypertensive medicine use differs between Ghana and Nigeria, Related Products of pyridine-derivatives, the main research area is (PubMed MESH terms); Antihypertensive medicines; Ghana; Hypertension; Nigeria; Pharmacoepidemiology.

Abstract: Background: Non-communicable diseases are a growing burden in many African countries; cardiovascular disease is the main disease. Antihypertensive medicines (AHM) are a common treatment option but we know little about community use in most low- and medium-income countries (LMIC). We aimed to describe the use of antihypertensive medicines (AHM) in Ghana and Nigeria using a novel data source. Methods: We used data from mPharma-a health and pharmaceutical company which distributes pharmaceuticals to hospital and retail pharmacies. We extracted data using the anatomical therapeutic chem. (ATC) classification codes and calculated use in defined daily doses and explored patterns by class, medicines, dose, and originator or generic product. Results: AHM use differed between Ghana and Nigeria. The most used classes in Ghana were angiotensin receptor blockers (ARB) followed by calcium channel blockers (CCB) and angiotensin-converting-enzyme inhibitors (ACEi). The five most used products were 16 mg candesartan, 30 mg nifedipine, 10 mg lisinopril, 5 mg amlodipine and 50 mg losartan. In Nigeria ARB, CCB and diuretics were widely used; the top five products were 50 mg losartan, 10 mg lisinopril, 30 mg nifedipine, 40 mg furosemide, and 5 mg amlodipine. More originator products were used in Ghana than Nigeria. Conclusion: The differences between Ghana and Nigeria may result from a combination of medical, contextual and policy evidence and reflect factors related to clin. guidance (e.g. standard treatment guidelines), accessibility to prescribers and the role of community pharmacies, and structure of the health system and universal health coverage including funding for medicines. We show the feasibility of using novel data sources to gain insights on medicines use in the community.

BMC Cardiovascular Disorders published new progress about (PubMed MESH terms); Antihypertensive medicines; Ghana; Hypertension; Nigeria; Pharmacoepidemiology. 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

Jayant, Satyam Singh published the artcileTriple A (Allgrove) syndrome due to AAAS gene mutation with a rare association of amyotrophy., COA of Formula: C17H18N2O6, the main research area is AAAS gene; ACTH resistance; Achalasia; Amyotrophy; Triple A syndrome.

INTRODUCTION: Triple A (Allgrove) syndrome is a rare autosomal recessive disorder characterized by cardinal features of primary adrenal insufficiency (AI) due to adrenocorticotropic hormone (ACTH) resistance, achalasia, and alacrima. It is frequently associated with neurological manifestations such as autonomic dysfunction, cognitive dysfunction, cranial nerve, or motor involvement. Amyotrophy/motor neuron disease is a rare association. CASE PRESENTATION: We herein report a 19-year-old boy diagnosed with triple A syndrome (TAS), with the classic triad of ACTH-resistant adrenal insufficiency, achalasia, and alacrima. Additionally, he had distal spinal muscle amyotrophy. Alacrima was the earliest feature evident in early childhood, followed by achalasia at 12 years of age. He was diagnosed with AI at the age of 19 years, with involvement of the mineralocorticoid axis. Further evaluation showed a neurogenic pattern on electromyography, consistent with a diagnosis of motor neuron disease. A nerve conduction study revealed no significant neuropathy. Genetic analysis confirmed a pathogenic homozygous mutation in the AAAS gene c.43C>A, p.Gln15Lys. He improved with glucocorticoid and mineralocorticoid supplements for AI, and nifedipine for achalasia and artificial tears. He is planned for esophagomyotomy. CONCLUSION: In any young patient with AI not due to congenital adrenal hyperplasia, Allgrove syndrome should be ruled out. Though mineralocorticoid sparing pattern is classical, it can rarely be involved, as seen in the index case. Various components of the syndrome, as well as amyotrophy and other neurologic features, may present in a metachronous fashion. Hence, a high index of clinical suspicion can aid in early diagnosis and management.

Hormones (Athens, Greece) published new progress about AAAS gene; ACTH resistance; Achalasia; Amyotrophy; Triple A syndrome. 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, COA of Formula: C17H18N2O6.

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Bhattarai, Anjan published the artcileDelayed-Onset High Altitude Pulmonary Edema: A Case Report., Synthetic Route of 21829-25-4, the main research area is acetazolamide; acute mountain sickness; altitude illness.

High altitude pulmonary edema (HAPE) is a life-threatening altitude illness that usually occurs in insufficiently acclimatized climbers in the first few days at altitudes above 2500 m. Acetazolamide is recommended for prophylaxis of acute mountain sickness, but a role for acetazolamide in the prevention of HAPE has not been established. We report a case of a trekker with previous high altitude experience who developed HAPE 8 d after arrival to altitude despite what was believed to be a conservative ascent profile.

Wilderness & environmental medicine published new progress about acetazolamide; acute mountain sickness; altitude illness. 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

Luks, Andrew M published the artcileCOVID-19 Lung Injury and High-Altitude Pulmonary Edema. A False Equation with Dangerous Implications., Application of Dimethyl 2,6-dimethyl-4-(2-nitrophenyl)-1,4-dihydropyridine-3,5-dicarboxylate, the main research area is acetazolamide; acute respiratory distress syndrome; coronavirus disease; high-altitude pulmonary edema; nifedipine.

Amid efforts to care for the large number of patients with coronavirus disease (COVID-19), there has been considerable speculation about whether the lung injury seen in these patients is different than acute respiratory distress syndrome from other causes. One idea that has garnered considerable attention, particularly on social media and in free open-access medicine, is the notion that lung injury due to COVID-19 is more similar to high-altitude pulmonary edema (HAPE). Drawing on this concept, it has also been proposed that treatments typically employed in the management of HAPE and other forms of acute altitude illness-pulmonary vasodilators and acetazolamide-should be considered for COVID-19. Despite some similarities in clinical features between the two entities, such as hypoxemia, radiographic opacities, and altered lung compliance, the pathophysiological mechanisms of HAPE and lung injury due to COVID-19 are fundamentally different, and the entities cannot be viewed as equivalent. Although of high utility in the management of HAPE and acute mountain sickness, systemically delivered pulmonary vasodilators and acetazolamide should not be used in the treatment of COVID-19, as they carry the risk of multiple adverse consequences, including worsened ventilation-perfusion matching, impaired carbon dioxide transport, systemic hypotension, and increased work of breathing.

Annals of the American Thoracic Society published new progress about acetazolamide; acute respiratory distress syndrome; coronavirus disease; high-altitude pulmonary edema; nifedipine. 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

Thakur, Monika published the artcileTo study the changes in maternal hemodynamics with intravenous labetalol or nifedipine in acute severe hypertension., Product Details of C17H18N2O6, the main research area is Acute severe hypertension; Doppler; Intravenous labetalol; Nifedipine; Pregnancy; Renal artery; Uterine artery.

OBJECTIVE: To study the maternal hemodynamic changes in acute severe hypertension after treatment with intravenous labetalol or oral nifedipine using color doppler ultrasound. STUDY DESIGN: We evaluated thirty pregnant women with gestational age between 28 and 40 weeks in acute severe hypertension (more than or equal to 160/105 mmHg) which were randomly allocated to receive either intravenous labetalol or oral nifedipine until blood pressure was lowered to less than or equal to 140/90 mmHg. Doppler vascular indices namely pulsatility index, resistance index, S/D ratio of bilateral uterine arteries and maternal renal artery were measured baseline at the time of acute severe hypertension and repeated after control of blood pressure, to assess the changes in maternal hemodynamics if any with labetalol or nifedipine. RESULTS: When evaluating right uterine artery Doppler parameters, a trend to increase in PI and RI was observed in those who received labetalol and nifedipine however the difference was not statistically significant. Whereas, while evaluating left uterine artery indices a trend to decrease PI was seen in nifedipine group but the difference was not statistically significant. On intergroup comparison there was no any significant change in any of uterine artery as well as renal artery indices in either group. CONCLUSION: The use of labetalol and nifedipine were not related to any significant changes in maternal Doppler, which is reassuring about the safety of these drugs when treating acute severe hypertension in pregnancy.

Pregnancy hypertension published new progress about Acute severe hypertension; Doppler; Intravenous labetalol; Nifedipine; Pregnancy; Renal artery; Uterine artery. 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