Effects of Acute Stress on Thrombosis

2018 ◽  
Vol 44 (07) ◽  
pp. 662-668 ◽  
Author(s):  
Ohad Bentur ◽  
Galit Sarig ◽  
Benjamin Brenner ◽  
Giris Jacob
Keyword(s):  
Human Body ◽  
Adaptive Response ◽  
Acute Stress ◽  
Epidemiological Studies ◽  
Neural System ◽  
Stress Reaction ◽  
Coagulation Cascade ◽  
Thrombotic Risk ◽  
The Relationship ◽  
Pituitary Adrenal Axis

AbstractStress, the nonspecific response to any demand for change, is an adaptive response of the human body to various stimulants. As such, stress-induced hypercoagulation may represent an adaptive response to bleeding. Numerous epidemiological studies have revealed that a correlation exists between stress and thrombotic risk and biochemically, links of the relationship between psychological stress and coagulation pathways have been made. The stress reaction is coupled with neurohormonal changes mediated mainly by the sympathetic neural system and the hypothalamic–pituitary–adrenal axis. Singling out the specific pathways affecting coagulation in this complex response is hampered by many confounders. The mediators of the stress reaction (neurotransmitters and hormones) can directly affect platelets and the coagulation cascade and indirectly affect hemostasis via changes in hemodynamics. In this review, the authors will delineate the distinct neurobiological mechanisms that govern the effects of stress on coagulation, and report their recent findings.

The Neurochemistry and Epigenetics of PTSD

2018 ◽  
Author(s):  
Robert M. Post
Keyword(s):  
Early Life ◽  
Stress Disorder ◽  
Acute Stress ◽  
Stress Reaction ◽  
Moving Target ◽  
Acute Stress Reaction ◽  
Life Stressor ◽  
The Common ◽  
Early Life Stressor ◽  
Pituitary Adrenal Axis

This chapter reviews the neurochemistry and epigenetics of posttraumatic stress disorder (PTSD). Traditional views of the neurochemistry of PTSD focus on alterations in classical central nervous system neurotransmitters serotonin and norepinephrine and pathological reactivity in the hypothalamic-pituitary-adrenal axis, and these are only briefly noted here. Instead, the chapter emphasizes a series of new conceptualizations and neurochemical data that have recently been elucidated. One is the recognition of the symptoms and neurobiology of PTSD as a moving target, being very different in different stages of illness evolution. Differences are apparent in the neurochemistry involved in early life stressor-related vulnerabilities to PTSD, the acute stress reaction, compensation and resolution phases, or ongoing chronicity with sleep disturbance, nightmares, flashbacks, hyperarousal, and dulling and depression. The neurochemical abnormalities vary as a function of this temporal unfolding and the common acquisition and progression of comorbid syndromes of alcohol and substance abuse.

Correction of Posture Deviations in the Sagittal Plane Using the Pilates Method

2019 ◽  
pp. 3-13
Author(s):  
Alexandru Cîtea ◽  
George-Sebastian Iacob
Keyword(s):  
Low Back Pain ◽  
Back Pain ◽  
Postural Control ◽  
Human Body ◽  
Sagittal Plane ◽  
The Body ◽  
Lower Limbs ◽  
Low Back ◽  
Pilates Method ◽  
The Relationship

Posture is commonly perceived as the relationship between the segments of the human body upright. Certain parts of the body such as the cephalic extremity, neck, torso, upper and lower limbs are involved in the final posture of the body. Musculoskeletal instabilities and reduced postural control lead to the installation of nonstructural posture deviations in all 3 anatomical planes. When we talk about the sagittal plane, it was concluded that there are 4 main types of posture deviation: hyperlordotic posture, kyphotic posture, rectitude and "sway-back" posture.Pilates method has become in the last decade a much more popular formof exercise used in rehabilitation. The Pilates method is frequently prescribed to people with low back pain due to their orientation on the stabilizing muscles of the pelvis. Pilates exercise is thus theorized to help reactivate the muscles and, by doingso, increases lumbar support, reduces pain, and improves body alignment.

Potential Role of Inflammation in Associations between Particulate Matter and Heart Failure

2018 ◽  
Vol 24 (3) ◽  
pp. 341-358 ◽  
Author(s):  
Xiaotong Ji ◽  
Yingying Zhang ◽  
Guangke Li ◽  
Nan Sang
Keyword(s):  
Heart Failure ◽  
Particulate Matter ◽  
Inflammatory Response ◽  
Heart Diseases ◽  
Experimental Studies ◽  
Epidemiological Studies ◽  
Inflammatory Mechanism ◽  
High Concentrations ◽  
Future Work ◽  
The Relationship

Recently, numerous studies have found that particulate matter (PM) exposure is correlated with increased hospitalization and mortality from heart failure (HF). In addition to problems with circulation, HF patients often display high expression of cytokines in the failing heart. Thus, as a recurring heart problem, HF is thought to be a disorder characterized in part by the inflammatory response. In this review, we intend to discuss the relationship between PM exposure and HF that is based on inflammatory mechanism and to provide a comprehensive, updated evaluation of the related studies. Epidemiological studies on PM-induced heart diseases are focused on high concentrations of PM, high pollutant load exposure in winter, or susceptible groups with heart diseases, etc. Furthermore, it appears that the relationship between fine or ultrafine PM and HF is stronger than that between HF and coarse PM. However, fewer studies paid attention to PM components. As for experimental studies, it is worth noting that coarse PM may indirectly promote the inflammatory response in the heart through systematic circulation of cytokines produced primarily in the lungs, while ultrafine PM and its components can enter circulation and further induce inflammation directly in the heart. In terms of PM exposure and enhanced inflammation during the pathogenesis of HF, this article reviews the following mechanisms: hemodynamics, oxidative stress, Toll-like receptors (TLRs) and epigenetic regulation. However, many problems are still unsolved, and future work will be needed to clarify the complex biologic mechanisms and to identify the specific components of PM responsible for adverse effects on heart health.

Adolescent smoking behavior and communication with parents: Depression as a mediator and gender as a moderator

2019 ◽  
Vol 47 (10) ◽  
pp. 1-9 ◽  
Author(s):  
Xieping Chen ◽  
Qian Xie ◽  
Yuting Yang
Keyword(s):  
Smoking Behavior ◽  
Depression Scale ◽  
Epidemiological Studies ◽  
Adolescent Smoking ◽  
Junior High Schools ◽  
Test Results ◽  
Negative Effect ◽  
And Gender ◽  
The Relationship ◽  
Communication Scale

Parent–adolescent communication is assumed to be an important factor affecting adolescent smoking behavior. However, the inner mechanism accounting for this association has still not been clarified in research. Our purpose in this study was to examine the relationships between parent–adolescent communication, adolescent smoking behavior, and depression, as well as gender differences in the relationship between depression and adolescent smoking behavior. Participants were 1,134 students at 6 junior high schools in China who completed the Parent-Adolescent Communication Scale, the Epidemiological Studies Depression Scale, and the Smoking Behavior Test. Results showed that parent-adolescent communication had a significant negative effect on adolescent smoking behavior and depression partially mediated the relationship between parent–adolescent communication and adolescent smoking behavior. In addition, gender moderated the relationship between depression and adolescent smoking behavior. Overall, these findings may help to promote better understanding of the relationship between parent–adolescent communication and adolescent smoking behavior.

scholarly journals Uric Acid and Hypertension: Prognostic Role and Guide for Treatment

2021 ◽  
Vol 10 (3) ◽  
pp. 448
Author(s):  
Federica Piani ◽  
Arrigo F. G. Cicero ◽  
Claudio Borghi
Keyword(s):  
Clinical Trials ◽  
Uric Acid ◽  
Mendelian Randomization ◽  
Strong Association ◽  
Epidemiological Studies ◽  
Hypertensive Disease ◽  
Genetic Studies ◽  
Lowering Therapy ◽  
The Relationship

The relationship between serum uric acid (SUA) and hypertension has been a subject of increasing interest since the 1870 discovery by Frederick Akbar Mahomed. Several epidemiological studies have shown a strong association between high SUA levels and the presence or the development of hypertension. Genetic analyses have found that xanthine oxidoreductase (XOR) genetic polymorphisms are associated with hypertension. However, genetic studies on urate transporters and Mendelian randomization studies failed to demonstrate a causal relationship between SUA and hypertension. Results from clinical trials on the role of urate-lowering therapy in the management of patients with hypertension are not uniform. Our study sought to analyze the prognostic and therapeutic role of SUA in the hypertensive disease, from uric acid (UA) biology to clinical trials on urate-lowering therapies.

scholarly journals Lack of an association between gallstone disease and bilirubin levels with risk of colorectal cancer: a Mendelian randomisation analysis

2021 ◽  
Author(s):  
Richard Culliford ◽  
Alex J. Cornish ◽  
Philip J. Law ◽  
Susan M. Farrington ◽  
Kimmo Palin ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Large Scale ◽  
Causal Effect ◽  
Gallstone Disease ◽  
Epidemiological Studies ◽  
Mendelian Randomisation ◽  
Linear Relationships ◽  
Potential Risk Factors ◽  
The Relationship ◽  
Circulating Levels

Abstract Background Epidemiological studies of the relationship between gallstone disease and circulating levels of bilirubin with risk of developing colorectal cancer (CRC) have been inconsistent. To address possible confounding and reverse causation, we examine the relationship between these potential risk factors and CRC using Mendelian randomisation (MR). Methods We used two-sample MR to examine the relationship between genetic liability to gallstone disease and circulating levels of bilirubin with CRC in 26,397 patients and 41,481 controls. We calculated the odds ratio per genetically predicted SD unit increase in log bilirubin levels (ORSD) for CRC and tested for a non-zero causal effect of gallstones on CRC. Sensitivity analysis was applied to identify violations of estimator assumptions. Results No association between either gallstone disease (P value = 0.60) or circulating levels of bilirubin (ORSD = 1.00, 95% confidence interval (CI) = 0.96–1.03, P value = 0.90) with CRC was shown. Conclusions Despite the large scale of this study, we found no evidence for a causal relationship between either circulating levels of bilirubin or gallstone disease with risk of developing CRC. While the magnitude of effect suggested by some observational studies can confidently be excluded, we cannot exclude the possibility of smaller effect sizes and non-linear relationships.

Endocannabinoid reactivity to acute stress: Investigation of the relationship between salivary and plasma levels

2021 ◽  
Vol 159 ◽  
pp. 108022
Author(s):  
Luke Ney ◽  
Caleb Stone ◽  
David Nichols ◽  
Kim Felmingham ◽  
Raimondo Bruno ◽  
...  
Keyword(s):  
Plasma Levels ◽  
Acute Stress ◽  
The Relationship

scholarly journals Human Elimination of Organochlorine Pesticides: Blood, Urine, and Sweat Study

2016 ◽  
Vol 2016 ◽  
pp. 1-10 ◽  
Author(s):  
Stephen J. Genuis ◽  
Kevin Lane ◽  
Detlef Birkholz
Keyword(s):  
Human Body ◽  
Urine Analysis ◽  
Epidemiological Studies ◽  
Metabolic Function ◽  
Endosulfan Sulfate ◽  
Clinical Tool ◽  
Organochlorinated Pesticides ◽  
Dual Column ◽  
Electron Capture Detectors ◽  
Serum Testing

Background. Many individuals have been exposed to organochlorinated pesticides (OCPs) through food, water, air, dermal exposure, and/or vertical transmission. Due to enterohepatic reabsorption and affinity to adipose tissue, OCPs are not efficiently eliminated from the human body and may accrue in tissues. Many epidemiological studies demonstrate significant exposure-disease relationships suggesting OCPs can alter metabolic function and potentially lead to illness. There is limited study of interventions to facilitate OCP elimination from the human body. This study explored the efficacy of induced perspiration as a means to eliminate OCPs.Methods. Blood, urine, and sweat (BUS) were collected from 20 individuals. Analysis of 23 OCPs was performed using dual-column gas chromatography with electron-capture detectors.Results. Various OCPs and metabolites, including DDT, DDE, methoxychlor, endrin, and endosulfan sulfate, were excreted into perspiration. Generally, sweat samples showed more frequent OCP detection than serum or urine analysis. Many OCPs were not readily detected in blood testing while still being excreted and identified in sweat. No direct correlation was found among OCP concentrations in the blood, urine, or sweat compartments.Conclusions. Sweat analysis may be useful in detecting some accrued OCPs not found in regular serum testing. Induced perspiration may be a viable clinical tool for eliminating some OCPs.

scholarly journals Relationship between NAFLD and Periodontal Disease from the View of Clinical and Basic Research, and Immunological Response

2021 ◽  
Vol 22 (7) ◽  
pp. 3728
Author(s):  
Masahiro Hatasa ◽  
Sumiko Yoshida ◽  
Hirokazu Takahashi ◽  
Kenichi Tanaka ◽  
Yoshihito Kubotsu ◽  
...  
Keyword(s):  
Risk Factor ◽  
Periodontal Disease ◽  
Alveolar Bone ◽  
Basic Research ◽  
Epidemiological Studies ◽  
Cross Sectional ◽  
Periodontopathic Bacteria ◽  
In Vivo Animal Model ◽  
The Relationship

Periodontal disease is an inflammatory disease caused by pathogenic oral microorganisms that leads to the destruction of alveolar bone and connective tissues around the teeth. Although many studies have shown that periodontal disease is a risk factor for systemic diseases, such as type 2 diabetes and cardiovascular diseases, the relationship between nonalcoholic fatty liver disease (NAFLD) and periodontal disease has not yet been clarified. Thus, the purpose of this review was to reveal the relationship between NAFLD and periodontal disease based on epidemiological studies, basic research, and immunology. Many cross-sectional and prospective epidemiological studies have indicated that periodontal disease is a risk factor for NAFLD. An in vivo animal model revealed that infection with periodontopathic bacteria accelerates the progression of NAFLD accompanied by enhanced steatosis. Moreover, the detection of periodontopathic bacteria in the liver may demonstrate that the bacteria have a direct impact on NAFLD. Furthermore, Porphyromonas gingivalis lipopolysaccharide induces inflammation and accumulation of intracellular lipids in hepatocytes. Th17 may be a key molecule for explaining the relationship between periodontal disease and NAFLD. In this review, we attempted to establish that oral health is essential for systemic health, especially in patients with NAFLD.

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