Quinidine-induced potentiation of cardiovascular effects of nitrendipine: functional aspects and possible molecular mechanisms

1995 ◽  
Vol 351 (6) ◽  
Author(s):  
Stefan Herzig ◽  
Julia Jischa ◽  
Antje Beinhauer ◽  
Bettina Geirhos ◽  
Kristin Tacke ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Cardiovascular Effects ◽  
Functional Aspects

Calciotropic and Magnesiotropic TRP Channels

Physiology ◽  
2008 ◽  
Vol 23 (1) ◽  
pp. 32-40 ◽  
Author(s):  
Joost G. J. Hoenderop ◽  
René J. M. Bindels
Keyword(s):  
Divalent Cation ◽  
Molecular Mechanisms ◽  
Transient Receptor Potential ◽  
Trp Channels ◽  
Receptor Potential ◽  
Transient Receptor Potential Channel ◽  
Significant Progress ◽  
Functional Aspects ◽  
Health And Disease ◽  
Transient Receptor

Significant progress has been made into our understanding of the molecular mechanisms responsible for Ca2+ and Mg2+ homeostasis. Members of the transient receptor potential channel (TRP) superfamily proved essential to the maintenance of divalent cation levels by regulating their absorption from renal and intestinal lumina. This review highlights the molecular and functional aspects of these new calciotropic and magnesiotropic TRPs in health and disease.

Cardiovascular Effects of Cocaine: Cellular, Ionic and Molecular Mechanisms

2012 ◽  
Vol 19 (33) ◽  
pp. 5664-5676 ◽  
Author(s):  
E. Turillazzi ◽  
S. Bello ◽  
M. Neri ◽  
C. Pomara ◽  
I. Riezzo ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Cardiovascular Effects

scholarly journals ROS in Platelet Biology: Functional Aspects and Methodological Insights

2020 ◽  
Vol 21 (14) ◽  
pp. 4866 ◽  
Author(s):  
Elena Masselli ◽  
Giulia Pozzi ◽  
Mauro Vaccarezza ◽  
Prisco Mirandola ◽  
Daniela Galli ◽  
...  
Keyword(s):  
Platelet Activation ◽  
Molecular Mechanisms ◽  
Redox Balance ◽  
Ros Production ◽  
Thrombotic Risk ◽  
Disease Biomarkers ◽  
Redox Biology ◽  
Napdh Oxidase ◽  
Functional Aspects ◽  
Platelet Functions

Reactive oxygen species (ROS) and mitochondria play a pivotal role in regulating platelet functions. Platelet activation determines a drastic change in redox balance and in platelet metabolism. Indeed, several signaling pathways have been demonstrated to induce ROS production by NAPDH oxidase (NOX) and mitochondria, upon platelet activation. Platelet-derived ROS, in turn, boost further ROS production and consequent platelet activation, adhesion and recruitment in an auto-amplifying loop. This vicious circle results in a platelet procoagulant phenotype and apoptosis, both accounting for the high thrombotic risk in oxidative stress-related diseases. This review sought to elucidate molecular mechanisms underlying ROS production upon platelet activation and the effects of an altered redox balance on platelet function, focusing on the main advances that have been made in platelet redox biology. Furthermore, given the increasing interest in this field, we also describe the up-to-date methods for detecting platelets, ROS and the platelet bioenergetic profile, which have been proposed as potential disease biomarkers.

scholarly journals Cardiovascular Effects and Molecular Mechanisms of Bisphenol A and Its Metabolite MBP in Zebrafish

2018 ◽  
Vol 53 (1) ◽  
pp. 463-474 ◽  
Author(s):  
A. Ross Brown ◽  
Jon M. Green ◽  
John Moreman ◽  
Lina M. Gunnarsson ◽  
Sulayman Mourabit ◽  
...  
Keyword(s):  
Bisphenol A ◽  
Molecular Mechanisms ◽  
Cardiovascular Effects

scholarly journals A Novel Promising Frontier for Human Health: The Beneficial Effects of Nutraceuticals in Cardiovascular Diseases

2020 ◽  
Vol 21 (22) ◽  
pp. 8706
Author(s):  
Albino Carrizzo ◽  
Carmine Izzo ◽  
Maurizio Forte ◽  
Eduardo Sommella ◽  
Paola Di Pietro ◽  
...  
Keyword(s):  
Cardiovascular Diseases ◽  
Human Health ◽  
Molecular Mechanisms ◽  
Cardiovascular Health ◽  
Public Health Problem ◽  
Cardiovascular Effects ◽  
Beneficial Effects ◽  
Significant Public Health ◽  
Health Promoting ◽  
The Individual

Cardiovascular diseases (CVDs) such as hypertension, atherosclerosis, myocardial infarction, and diabetes are a significant public health problem worldwide. Although several novel pharmacological treatments to reduce the progression of CVDs have been discovered during the last 20 years, the better way to contain the onset of CVDs remains prevention. In this regard, nutraceuticals seem to own a great potential in maintaining human health, exerting important protective cardiovascular effects. In the last years, there has been increased focus on identifying natural compounds with cardiovascular health-promoting effects and also to characterize the molecular mechanisms involved. Although many review articles have focused on the individual natural compound impact on cardiovascular diseases, the aim of this manuscript was to examine the role of the most studied nutraceuticals, such as resveratrol, cocoa, quercetin, curcumin, brassica, berberine and Spirulina platensis, on different CVDs.

scholarly journals Penetrating Ballistic Brain Injury Produces Acute Alterations in Sleep and Circadian-Related Genes in the Rodent Cortex: A Preliminary Study

2021 ◽  
Vol 12 ◽  
Author(s):  
Andrea Mountney ◽  
Jennifer Blaze ◽  
Zhaoyu Wang ◽  
Michelle Umali ◽  
William Jesse Flerlage ◽  
...  
Keyword(s):  
Brain Injury ◽  
Sleep Disturbance ◽  
Molecular Mechanisms ◽  
Slow Wave Sleep ◽  
Transcriptional Profiling ◽  
Cardiovascular Effects ◽  
Sleep Stages ◽  
Post Injury ◽  
Novel Treatments ◽  
Wide Range

Traumatic brain injury (TBI) affects millions of Americans each year, with extremely high prevalence in the Veteran community, and sleep disturbance is one of the most commonly reported symptoms. Reduction in the quality and amount of sleep can negatively impact recovery and result in a wide range of behavioral and physiological symptoms, such as impaired cognition, mood and anxiety disorders, and cardiovascular effects. Thus, to improve long-term patient outcomes and develop novel treatments, it is essential to understand the molecular mechanisms involved in sleep disturbance following TBI. In this effort, we performed transcriptional profiling in an established rodent model of penetrating ballistic brain injury (PBBI) in conjunction with continuous sleep/wake EEG/EMG recording of the first 24 h after injury. Rats subjected to PBBI showed profound differences in sleep architecture. Injured animals spent significantly more time in slow wave sleep and less time in REM sleep compared to sham control animals. To identify PBBI-related transcriptional differences, we then performed transcriptome-wide gene expression profiling at 24 h post-injury, which identified a vast array of immune- related genes differentially expressed in the injured cortex as well as sleep-related genes. Further, transcriptional changes associated with total time spent in various sleep stages were identified. Such molecular changes may underlie the pathology and symptoms that emerge following TBI, including neurodegeneration, sleep disturbance, and mood disorders.

Non-opioid analgesics

2015 ◽  
Author(s):  
Per Sjøgren ◽  
Frank Elsner ◽  
Stein Kaasa
Keyword(s):  
Molecular Mechanisms ◽  
Cardiovascular Effects ◽  
Opioid Analgesics ◽  
Mechanisms Of Action ◽  
World Health ◽  
Antipyretic Activity ◽  
Increased Risk ◽  
Recent Developments ◽  
Inflammatory Drugs ◽  
Anti Inflammatory

Non-opioid analgesics encompass the non-steroidal anti-inflammatory drugs (NSAIDs) and paracetamol (acetaminophen). The NSAIDs include acetylsalicylic acid (ASA, aspirin), dipyrone (metamizole), and numerous other drugs in diverse classes. The NSAIDs have potent anti-inflammatory, analgesic and antipyretic activity, and are among the most widely used drugs worldwide. In palliative medicine, they represent the first step of the World Health Organization’s analgesic ladder used for mild pain and they are an important supplement to opioids and adjuvant drugs at higher steps of the ladder. The disadvantages of non-opioid analgesics include a ceiling effect for pain relief and the risk of side effects. NSAIDs are also associated with an increased risk of adverse gastrointestinal, renal, and cardiovascular effects and hepatotoxicity can result from overdosing with paracetamol. This chapter describes the clinical pharmacology of NSAIDs, their classification, molecular mechanisms of action and adverse effects, as well as some recent developments aimed at designing effective anti-inflammatory agents with improved safety and tolerability profiles.

scholarly journals On the chromatin of the immature oocyte: from morphology to function and regulatory mechanisms mediated by follicular cells

2015 ◽  
Author(s):  
Valentina Lodde ◽  
Silvia C. Modina ◽  
Alberto M. Luciano
Keyword(s):  
Cell Biology ◽  
Molecular Mechanisms ◽  
Functional Aspects ◽  
Complex Process ◽  
Chromatin Configuration ◽  
Oocyte Differentiation ◽  
The Relationship ◽  
Insight Into ◽  
Tremendous Impact

In her comment entitled ‘Nuclear histochemistry: its history in fifty volumes’ (Eur J Histochem 2006; 50:79-81) Maria Gabriella Manfredi Romanini referred to “nuclear histochemistry” as a “real molecular biology in situ, applied to research on dynamic processes in the nucleus, which makes the microscopic and histochemical approach absolutely irreplaceable for the progress of our understanding of cell biology”. These words perfectly exemplify the research path that is elucidating the process of remodeling of chromatin configuration within the nucleus of the mammalian oocyte. This process, which occurs towards the end of the oocyte differentiation phase before meiotic resumption, has received much attention in the last decade since it has a tremendous impact on the capability of the oocyte to generate an embryo after fertilization. The study of the oocyte chromatin by means of classical morphological and histochemical approaches has given a fundamental contribution to our understanding of oocyte biology and has paved the way to functional and mechanistic studies. Several research groups worldwide, including ours, are indeed dedicating a large amount of studies to find the relationship between morphological and functional aspects of the oocyte chromatin remodeling process, to reveal the molecular mechanisms involved, as well as to clarify the contribution of the follicular compartment. Here, we summarize some studies intended to give insight into the mechanism( s) regulating this complex process, including recent findings indicating that ovarian granulosa cells and their coupling with the oocyte through gap junctions are implicated in such a process.

scholarly journals Functional Aspects of Early Light-Induced Protein (ELIP) Genes from the Desiccation-Tolerant Moss Syntrichia caninervis

2020 ◽  
Vol 21 (4) ◽  
pp. 1411
Author(s):  
Xiujin Liu ◽  
Yigong Zhang ◽  
Honglan Yang ◽  
Yuqing Liang ◽  
Xiaoshuang Li ◽  
...  
Keyword(s):  
Molecular Mechanisms ◽  
Light Stress ◽  
Red Light ◽  
Ectopic Expression ◽  
Photosynthetic Apparatus ◽  
Transcript Abundance ◽  
High Light ◽  
Syntrichia Caninervis ◽  
Leaf Chlorophyll ◽  
Functional Aspects

The early light-induced proteins (ELIPs) are postulated to act as transient pigment-binding proteins that protect the chloroplast from photodamage caused by excessive light energy. Desert mosses such as Syntrichia caninervis, that are desiccation-tolerant and homoiochlorophyllous, are often exposed to high-light conditions when both hydrated and dry ELIP transcripts are accumulated in response to dehydration. To gain further insights into ELIP gene function in the moss S. caninervis, two ELIP cDNAs cloned from S. caninervis, ScELIP1 and ScELIP2 and both sequences were used as the basis of a transcript abundance assessment in plants exposed to high-light, UV-A, UV-B, red-light, and blue-light. ScELIPs were expressed separately in an Arabidopsis ELIP mutant Atelip. Transcript abundance for ScELIPs in gametophytes respond to each of the light treatments, in similar but not in identical ways. Ectopic expression of either ScELIPs protected PSII against photoinhibition and stabilized leaf chlorophyll content and thus partially complementing the loss of AtELIP2. Ectopic expression of ScELIPs also complements the germination phenotype of the mutant and improves protection of the photosynthetic apparatus of transgenic Arabidopsis from high-light stress. Our study extends knowledge of bryophyte photoprotection and provides further insight into the molecular mechanisms related to the function of ELIPs.

scholarly journals A LONGEVITY PROMOTING FACTOR THAT SUPPRESSES IMMUNITY AND HEALTHSPAN

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S769-S769
Author(s):  
Arjumand Ghazi ◽  
Francis Amrit ◽  
Nikki Naim ◽  
Ramesh Ratnappan ◽  
Julia Loose ◽  
...  
Keyword(s):  
Stress Resistance ◽  
Molecular Mechanisms ◽  
Opportunistic Pathogen ◽  
Coupled Processes ◽  
C Elegans ◽  
Susceptibility To Infection ◽  
Abiotic Stressors ◽  
Functional Aspects ◽  
Length Of Life ◽  
Increased Susceptibility

Abstract A positive correlation exists between stress resistance and longevity, but emerging evidence suggests that lifespan and stress endurance are physiologically distinct. A major challenge in aging biology has been identifying factors that play distinct roles in these closely coupled processes because genes that promote longevity often enhance stress resistance. Here, we demonstrate that TCER-1, the Caenorhabditis elegans homolog of the human transcription elongation and splicing factor, TCERG1, has discrete and opposite effects on lifespan and stress resistance. We previously identified tcer-1 as a gene that promotes longevity in germline-less C. elegans and reproductive fitness in wild-type animals. Surprisingly, tcer-1 mutants exhibited exceptional resistance against multiple biotic and abiotic stressors, including infection by the human opportunistic pathogen Pseudomonas aeruginosa. Conversely, TCER-1 overexpression increased susceptibility to infection. TCER-1 acted cell non-autonomously to both enhance longevity and repress immunity. Interestingly, TCER-1 inhibited immunity only during the fertile stages of life and not in post-reproductive adults. Elevating its levels ameliorated the fertility loss that follows infection, suggesting that TCER-1 may repress immunity to augment fecundity. Mechanistically, TCER-1 acts through the inhibition of the conserved kinase, PMK-1, as well as through repression of PMK-1-independent, novel antibacterial factors critical for innate immunity. Overall, our data establish key roles for TCER-1 in coordinating immunity, longevity and fertility, and reveal the molecular mechanisms that distinguish length of life from functional aspects of aging.

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