scholarly journals Melatonin and Human Cardiovascular Disease

2016 ◽  
Vol 22 (2) ◽  
pp. 122-132 ◽  
Author(s):  
Seithikurippu R. Pandi-Perumal ◽  
Ahmed S. BaHammam ◽  
Nwakile I. Ojike ◽  
Oluwaseun A. Akinseye ◽  
Tetyana Kendzerska ◽  
...  
Keyword(s):  
Pulsatility Index ◽  
Internal Carotid ◽  
Cardiovascular Effects ◽  
Therapeutic Interventions ◽  
Cardiovascular Disorders ◽  
Nocturnal Hypertension ◽  
Circulating Levels ◽  
Catecholamine Levels ◽  
Novel Therapeutic

The possible therapeutic role of melatonin in the pathophysiology of coronary artery disorder (CAD) is increasingly being recognized. In humans, exogenous melatonin has been shown to decrease nocturnal hypertension, improve systolic and diastolic blood pressure, reduce the pulsatility index in the internal carotid artery, decrease platelet aggregation, and reduce serum catecholamine levels. Low circulating levels of melatonin are reported in individuals with CAD, arterial hypertension, and congestive heart failure. This review assesses current literature on the cardiovascular effects of melatonin in humans. It can be concluded that melatonin deserves to be considered in clinical trials evaluating novel therapeutic interventions for cardiovascular disorders.

scholarly journals Mitochondrial Function, Biology, and Role in Disease

2016 ◽  
Vol 118 (12) ◽  
pp. 1960-1991 ◽  
Author(s):  
Elizabeth Murphy ◽  
Hossein Ardehali ◽  
Robert S. Balaban ◽  
Fabio DiLisa ◽  
Gerald W. Dorn ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Mitochondrial Function ◽  
The United States ◽  
Therapeutic Interventions ◽  
Therapeutic Approaches ◽  
Mitochondrial Defects ◽  
Exciting Time ◽  
Insight Into ◽  
Novel Therapeutic

Cardiovascular disease is a major leading cause of morbidity and mortality in the United States and elsewhere. Alterations in mitochondrial function are increasingly being recognized as a contributing factor in myocardial infarction and in patients presenting with cardiomyopathy. Recent understanding of the complex interaction of the mitochondria in regulating metabolism and cell death can provide novel insight and therapeutic targets. The purpose of this statement is to better define the potential role of mitochondria in the genesis of cardiovascular disease such as ischemia and heart failure. To accomplish this, we will define the key mitochondrial processes that play a role in cardiovascular disease that are potential targets for novel therapeutic interventions. This is an exciting time in mitochondrial research. The past decade has provided novel insight into the role of mitochondria function and their importance in complex diseases. This statement will define the key roles that mitochondria play in cardiovascular physiology and disease and provide insight into how mitochondrial defects can contribute to cardiovascular disease; it will also discuss potential biomarkers of mitochondrial disease and suggest potential novel therapeutic approaches.

scholarly journals Velocity Pulsatility and Arterial Distensibility Along the Internal Carotid Artery

2020 ◽  
Vol 9 (16) ◽  
Author(s):  
Rick J. van Tuijl ◽  
Ynte M. Ruigrok ◽  
Birgitta K. Velthuis ◽  
Irene C. van der Schaaf ◽  
Gabriël J. E. Rinkel ◽  
...  
Keyword(s):  
Carotid Artery ◽  
Internal Carotid Artery ◽  
Pulsatility Index ◽  
Internal Carotid ◽  
Arterial Distensibility ◽  
Carotid Siphon ◽  
Carotid Canal ◽  
The Brain ◽  
Healthy Participants

Background Attenuation of velocity pulsatility along the internal carotid artery (ICA) is deemed necessary to protect the microvasculature of the brain. The role of the carotid siphon within the whole ICA trajectory in pulsatility attenuation is still poorly understood. This study aims to assess arterial variances in velocity pulsatility and distensibility over the whole ICA trajectory, including effects of age and sex. Methods and Results We assessed arterial velocity pulsatility and distensibility using flow‐sensitized 2‐dimensional phase‐contrast 3.0 Tesla magnetic resonance imaging in 118 healthy participants. Velocity pulsatility index (vPI=(V max −V min )/V mean ) and arterial distensibility defined as area pulsatility index (A max −A min )/A mean ) were calculated at C1, C3, and C7 segments of the ICA. vPI increased between C1 and C3 (0.85±0.13 versus 0.93±0.13, P <0.001 for averaged right+left ICA) and decreased between C3 and C7 (0.93±0.13 versus 0.84±0.13, P <0.001) with overall no effect (C1–C7). Conversely, the area pulsatility index decreased between C1 and C3 (0.18±0.06 versus 0.14±0.04, P <0.001) and increased between C3 and C7 (0.14±0.04 versus 0.31±0.09, P <0.001). vPI in men is higher than in women and increases with age ( P <0.015). vPI over the carotid siphon declined with age but remained stable over the whole ICA trajectory. Conclusions Along the whole ICA trajectory, vPI increased from extracranial C1 up to the carotid siphon C3 with overall no effect on vPI between extracranial C1 and intracranial C7 segments. This suggests that the bony carotid canal locally limits the arterial distensibility of the ICA, increasing the vPI at C3 which is consequently decreased again over the carotid siphon. In addition, vPI in men is higher and increases with age.

Role of oxidative stress in angiotensin-induced hypertension

2003 ◽  
Vol 284 (4) ◽  
pp. R893-R912 ◽  
Author(s):  
Jane F. Reckelhoff ◽  
J. Carlos Romero
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Sodium Intake ◽  
Therapeutic Interventions ◽  
Ang Ii ◽  
Slow Increase ◽  
Pathological Conditions ◽  
Vasoconstrictor Response ◽  
Circulating Levels

Infusion of ANG II at a rate not sufficient to evoke an immediate vasoconstrictor response, produces a slow increase in blood pressure. Circulating levels of ANG II may be within ranges found in normotensive individuals, although inappropriately high with respect to sodium intake. When ANG II levels are dissociated from sodium levels, oxidative stress (OXST) occurs, which can increase blood pressure by several mechanisms. These include inadequate production or reduction of bioavailability of nitric oxide, alterations in metabolism of arachidonic acid, resulting in an increase in vasoconstrictors and decrease in vasodilators, and upregulation of endothelin. This cascade of events appears to be linked, because ANG II hypertension can be blocked by inhibition of any factor located distally, blockade of ANG II, OXST, or endothelin. Such characteristics are shared by other models of hypertension, such as essential hypertension, hypertension induced by reduction in renal mass, and renovascular hypertension. Thus these findings are clinically important because they reveal 1) uncoupling between ANG II and sodium, which can trigger pathological conditions; 2) the various OXST mechanisms that may be involved in hypertension; and 3) therapeutic interventions for hypertension developed with the knowledge of the cascade involving OXST.

Role of Estrogens in Addiction-Related Learning

2020 ◽  
pp. 456-474
Author(s):  
Hanna Yousuf
Keyword(s):  
Sex Differences ◽  
Cocaine Abuse ◽  
Therapeutic Interventions ◽  
Sexually Dimorphic ◽  
Addictive Behaviors ◽  
Cocaine Seeking ◽  
Preclinical Work ◽  
Novel Therapeutic ◽  
Memory Enhancing

Females exhibit more vulnerability to cocaine abuse compared to males. Sexually dimorphic patterns of cocaine seeking have been observed in both humans and rodents during the different stages of the addiction cycle. While cocaine pharmacokinetics play a minimal role in driving sex differences in addictive behaviors, hormonal influences may be responsible for the reinforcing properties of cocaine in females. In particular, 17β‎-estradiol (E2), enhances performance in a variety of learning paradigms and may act to enhance the formation of drug-related learning. Paradoxically, preclinical work demonstrates that the memory-enhancing effects of E2 may also aid to suppress cocaine seeking via extinction training. In addition to discussing how E2 mediates cocaine use in females, this chapter provides neurobiological mechanisms underlying E2’s influence on cocaine addiction. Finally, this chapter discusses potential strategies for novel therapeutic interventions for female cocaine addicts.

Cholesterol and its Ayurvedic Complement – Depicting its role in Pathogenesis as well as Management of Diabetes

2017 ◽  
Vol 2 (3) ◽  
Author(s):  
Divya Kajaria
Keyword(s):  
Treatment Modality ◽  
Review Article ◽  
Therapeutic Interventions ◽  
Herbal Remedies ◽  
Natural Properties ◽  
Lipid Balance ◽  
Vast Area

Role of cholesterol in the pathogenesis of diabetes is the emergent are of research with full of potential; it not only open a vast area of therapeutic interventions but also can change the prevailing treatment modality. Ayurveda, the Indian system of medicine materialize the concept of lipocenteric approach for the management of diabetes even thousands of years back. According to Ayurveda, the natural properties of lipid are deranged that causes diabetes. It may prove beneficial to quest the search of herbal remedies that can harmonize the lipid balance and uproot the pathogenesis. In the presenting review article, role of cholesterol in the pathogenesis of diabetes is discussed along with detailed description of Ayurvedic concepts regarding pathogenesis and a brief description of herbal management.

The Role of Resilience in Sexual and Gender Minority Mental Health

2020 ◽  
pp. 428-442
Author(s):  
Dawn M. Szymanski ◽  
Kirsten A. Gonzalez
Keyword(s):  
Mental Health ◽  
Minority Stress ◽  
Quantitative Research ◽  
Social Stigma ◽  
Therapeutic Interventions ◽  
Future Research ◽  
Minority Mental Health ◽  
And Gender ◽  
Structural Levels

Many lesbian, gay, bisexual, transgender, and queer (LGBTQ) persons are able to persevere and flourish despite pervasive social stigma and minority stress based on their sexual orientation and gender identity. This chapter reviews the research on LGBTQ resilience that can occur at individual, interpersonal/family, community, and contextual/structural levels. The authors describe qualitative research that has examined pathways to resilience and positive LGBTQ identity. The authors also review quantitative research on LGBTQ resilience via mediator, moderator, and moderated mediation models. Variables are described that have been found to explain or buffer the links between external and internalized minority stressors and mental health outcomes. The authors review the small but growing body of research that has begun to examine the efficacy of therapeutic interventions aimed at promoting LGBTQ resilience. Limitations are discussed and directions for future research are suggested.

scholarly journals The possible role of Interleukin-6 as a regulator of insulin sensitivity in patients with neuromyelitis optica spectrum disorder

BMC Neurology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Zhila Maghbooli ◽  
Abdorreza Naser Moghadasi ◽  
Nasim Rezaeimanesh ◽  
Abolfazl Omidifar ◽  
Tarlan Varzandi ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Neuromyelitis Optica ◽  
Serum Levels ◽  
Spectrum Disorder ◽  
Control Group ◽  
Neuromyelitis Optica Spectrum Disorder ◽  
Downstream Signaling ◽  
Reduce Insulin Sensitivity ◽  
Circulating Levels

Abstract Background Neuromyelitis optica spectrum disorder (NMOSD) is associated with inflammatory mediators that may also trigger downstream signaling pathways leading to reduce insulin sensitivity. Methods We aimed to determine the risk association of hyperinsulinemia in NMOSD patients with seropositive AQP4-IgG and the serum levels of interleukin (IL)-6 and IL-17A compared with the control group. Serum levels of metabolic (Insulin, Fasting Blood Sugar (FBS), lipid profile) and inflammatory (IL-6 and IL-17) markers were assessed in 56 NMOSD patients and 100 controls. Results Hyperinsulinemia was more prevalent in NMOSD patients independent of age, sex and body mass index (BMI) (48.2% vs. 26%, p = 0.005) compared to control group. After adjusting age, sex and BMI, there was significant association between lower insulin sensitivity (IS) and NMOSD risk (95% CI: Beta = 0.73, 0.62 to 0.86, p = 0.0001). Circulating levels of IL-6 and IL-17 were higher in NMOSD patients, and only IL-6 had an effect modifier for the association between lower insulin sensitivity and NMOSD risk. Conclusions Our data suggests that inflammatory pathogenesis of NMOSD leads to hyperinsulinemia and increases the risk of insulin resistance.

scholarly journals Neonatal Immune System Ontogeny: The Role of Maternal Microbiota and Associated Factors. How Might the Non-Human Primate Model Enlighten the Path?

Vaccines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 584
Author(s):  
Natalia Nunez ◽  
Louis Réot ◽  
Elisabeth Menu
Keyword(s):  
Immune System ◽  
Mode Of Delivery ◽  
Microbial Colonization ◽  
Therapeutic Interventions ◽  
Primate Model ◽  
Neonatal Immune System ◽  
Gastrointestinal Colonization ◽  
The Impact ◽  
Human Primate

Interactions between the immune system and the microbiome play a crucial role on the human health. These interactions start in the prenatal period and are critical for the maturation of the immune system in newborns and infants. Several factors influence the composition of the infant’s microbiota and subsequently the development of the immune system. They include maternal infection, antibiotic treatment, environmental exposure, mode of delivery, breastfeeding, and food introduction. In this review, we focus on the ontogeny of the immune system and its association to microbial colonization from conception to food diversification. In this context, we give an overview of the mother–fetus interactions during pregnancy, the impact of the time of birth and the mode of delivery, the neonate gastrointestinal colonization and the role of breastfeeding, weaning, and food diversification. We further review the impact of the vaccination on the infant’s microbiota and the reciprocal case. Finally, we discuss several potential therapeutic interventions that might help to improve the newborn and infant’s health and their responses to vaccination. Throughout the review, we underline the main scientific questions that are left to be answered and how the non-human primate model could help enlighten the path.

scholarly journals Therapeutic Application of Monoclonal Antibodies in Pancreatic Cancer: Advances, Challenges and Future Opportunities

Cancers ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 1781
Author(s):  
Gustavo A. Arias-Pinilla ◽  
Helmout Modjtahedi
Keyword(s):  
Pancreatic Cancer ◽  
Monoclonal Antibodies ◽  
Antibody Therapy ◽  
Therapeutic Targets ◽  
Poor Response ◽  
Therapeutic Agents ◽  
Therapeutic Interventions ◽  
Western World ◽  
Wide Range ◽  
Novel Therapeutic

Pancreatic cancer remains as one of the most aggressive cancer types. In the absence of reliable biomarkers for its early detection and more effective therapeutic interventions, pancreatic cancer is projected to become the second leading cause of cancer death in the Western world in the next decade. Therefore, it is essential to discover novel therapeutic targets and to develop more effective and pancreatic cancer-specific therapeutic agents. To date, 45 monoclonal antibodies (mAbs) have been approved for the treatment of patients with a wide range of cancers; however, none has yet been approved for pancreatic cancer. In this comprehensive review, we discuss the FDA approved anticancer mAb-based drugs, the results of preclinical studies and clinical trials with mAbs in pancreatic cancer and the factors contributing to the poor response to antibody therapy (e.g. tumour heterogeneity, desmoplastic stroma). MAb technology is an excellent tool for studying the complex biology of pancreatic cancer, to discover novel therapeutic targets and to develop various forms of antibody-based therapeutic agents and companion diagnostic tests for the selection of patients who are more likely to benefit from such therapy. These should result in the approval and routine use of antibody-based agents for the treatment of pancreatic cancer patients in the future.

scholarly journals B Cells and Antibodies as Targets of Therapeutic Intervention in Neuromyelitis Optica Spectrum Disorders

2021 ◽  
Vol 14 (1) ◽  
pp. 37
Author(s):  
Jan Traub ◽  
Leila Husseini ◽  
Martin S. Weber
Keyword(s):  
B Cells ◽  
Neuromyelitis Optica ◽  
Plasma Cells ◽  
Treatment Options ◽  
Treatment Strategies ◽  
Therapeutic Interventions ◽  
Complement Factor ◽  
Major Subset ◽  
Spectrum Disorders

The first description of neuromyelitis optica by Eugène Devic and Fernand Gault dates back to the 19th century, but only the discovery of aquaporin-4 autoantibodies in a major subset of affected patients in 2004 led to a fundamentally revised disease concept: Neuromyelits optica spectrum disorders (NMOSD) are now considered autoantibody-mediated autoimmune diseases, bringing the pivotal pathogenetic role of B cells and plasma cells into focus. Not long ago, there was no approved medication for this deleterious disease and off-label therapies were the only treatment options for affected patients. Within the last years, there has been a tremendous development of novel therapies with diverse treatment strategies: immunosuppression, B cell depletion, complement factor antagonism and interleukin-6 receptor blockage were shown to be effective and promising therapeutic interventions. This has led to the long-expected official approval of eculizumab in 2019 and inebilizumab in 2020. In this article, we review current pathogenetic concepts in NMOSD with a focus on the role of B cells and autoantibodies as major contributors to the propagation of these diseases. Lastly, by highlighting promising experimental and future treatment options, we aim to round up the current state of knowledge on the therapeutic arsenal in NMOSD.

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