Prenatal stress and its role in children's pathology: historical aspects and the current status of the question (review of literature)

2020 ◽  
Vol 24 (3) ◽  
pp. 28-41
Author(s):  
A. A. Vyalkova ◽  
B. A. Frolov ◽  
E. V. Savelyeva ◽  
S. A. Chesnokova

The article presents an analysis of fundamental data on the problem of stress and its role in the development of stressful diseases. Scientific evidence on the role of stress in childhood pathology indicates the extreme pathogenetic significance of stress. It is proved that stress has three interconnected faces: stress as a link in the adaptation mechanism, stress as a link in the pathogenesis of diseases and adaptation to stressful situations as a natural prevention of stressful diseases. The scientific substantiation of the main evolutionarily determined role of stress as an adaptation link indicates the possibility of acquiring some degree of resistance to stressful situations. Prevention of reducing the excess of stress reactions and reducing the possibility of its transformation into a link in the pathogenesis of diseases limits the complex of mechanisms designated as a stress-limiting system. Important information is the development and coordination of the stress response, which is provided by a complex set of mechanisms of neuroendocrine regulation, united by the concept of “stress-implementing system”. The most common forms of stress are fetal hypoxia, metabolic disturbances, and toxic effects leading to uncontrolled oxidative stress at the cellular and tissue levels with the development of pregnancy complications, intrauterine growth retardation syndrome (IUGR), persistent changes and pathological conditions. As the fetus grows, the flow of oxygen and nutrients from the mother through the placenta increases, which is accompanied by an increased risk of the formation of pathologies of the brain, heart, liver and kidneys with the development of a multi-organ pathology in the subsequent life. It has been proven that oxidative stress combined with stress of malnutrition in the prenatal period increases the risk of endocrinopathies, kidney diseases, and a number of other chronic diseases in the adult state. In practical terms, the negative effects of stress are of particular interest. Early detection of psychosocial and sympathomimetic factors causing stress is the basis for the prevention of childhood pathology.

Author(s):  
Delia Nica-Badea ◽  
Aurelian Udristioiu

Background: Vitamin D has a widely acknowledged role in regulating the metabolism of calcium and phosphate, both essential to bone remodeling. However, numerous studies in recent decades have emphasized the association between low sun exposure and vitamin D deficiency, and an increased risk of extra-skeletal disorders such as cancer. Objective: This mini-review of literature aims to present an objective overview of several recent studies and meta-analyses evaluating the role of vitamin D in cancer prevention, its potential to improve cancer treatment outcomes, as well as the negative effects of vitamin D deficiencies. Methods: The antitumor effects of calcitriol and analogs in the treatment of cancer, either as single agents or in combination with other anticancer agents, are based on several mechanisms: inhibition of cancer cell proliferation and invasiveness, induction of differentiation and apoptosis, and promotion of angiogenesis, all recorded in a number of preclinical studies of several cancer types Results: The importance of VDR polymorphisms for individual malignancies remains a topic of debate. Contradictory effects have been recorded in recent studies, the results of which include positive associations of VDR when cumulated with other risk factors, both an increase and a decrease in cancer risks, as well as no correlation between VDR polymorphisms and individual malignancies.. Conclusion: The scientific evidence reviewed in this paper suggests that health care providers and individuals should consider increasing concentrations of 25 (OH) D through sensitive sun exposure and / or by supplementing with vitamin D to reduce cancer risk and, in combination with standard care, to treat cancer.


Author(s):  
Ramazan Mert Atan ◽  
Uğur Günşen

Inflammation usually occurs as a result of imbalances between pro-inflammatory and anti-inflammatory cytokines. Diet is one of the factors that play a role in their development and prevent them from developing. Therefore, it is important to determine the pro- and anti-inflammatory properties of foods. Diet is an important and modifiable determinant of chronic diseases. There is a lot of scientific evidence to support the fact that foods consumed have positive and negative effects on individuals' health. In addition to being effective whole of diet, it is seen that the food groups contained in the diet affect the inflammatory biomarkers separately. This section provides information about dietary inflammatory index (DII) and diets that are effective on inflammation.


2012 ◽  
Vol 2012 ◽  
pp. 1-7 ◽  
Author(s):  
Ayşe Balat ◽  
Mithat Büyükçelik

Human urotensin-II (hU-II) is one of the most potent vasoconstrictors in mammals. Although both hU-II and its receptor, GPR14, are detected in several tissues, kidney is a major source of U-II in humans. Recent studies suggest that U-II may have a possible autocrine/paracrine functions in kidney and may be an important target molecule in studying renal pathophysiology. It has several effects on tubular transport and probably has active role in renal hemodynamics. Although it is an important peptide in renal physiology, certain diseases, such as hypertension and glomerulonephritis, may alter the expression of U-II. As might be expected, oxidative stress, mediators, and inflammation are like a devil's triangle in kidney diseases, mostly they induce each other. Since there is a complex relationship between U-II and oxidative stress, and other mediators, such as transforming growth factorβ1 and angiotensin II, U-II is more than a mediator in glomerular diseases. Although it is an ancient peptide, known for 31 years, it looks like that U-II will continue to give new messages as well as raising more questions as research on it increases. In this paper, we mainly discuss the possible role of U-II on renal physiology and its effect on kidney diseases.


2020 ◽  
Vol 319 (4) ◽  
pp. L585-L595 ◽  
Author(s):  
Kielan Darcy McAlinden ◽  
Mathew Suji Eapen ◽  
Wenying Lu ◽  
Pawan Sharma ◽  
Sukhwinder Singh Sohal

In 2019, the United States experienced the emergence of the vaping-associated lung injury (VALI) epidemic. Vaping is now known to result in the development and progression of severe lung disease in the young and healthy. Lack of regulation on electronic cigarettes in the United States has resulted in over 2,000 patients and 68 deaths. We examine the clinical representation of VALI and the delve into the scientific evidence of how deadly exposure to electronic cigarettes can be. E-cigarette vapor is shown to affect numerous cellular processes, cellular metabolism, and cause DNA damage (which has implications for cancer). E-cigarette use is associated with a higher risk of developing crippling lung conditions such as chronic obstructive pulmonary disease (COPD), which would develop several years from now, increasing the already existent smoking-related burden. The role of vaping and virus susceptibility is yet to be determined; however, vaping can increase the virulence and inflammatory potential of several lung pathogens and is also linked to an increased risk of pneumonia. As it has emerged for cigarette smoking, great caution should also be given to vaping in relation to SARS-CoV-2 infection and the COVID-19 pandemic. Sadly, e-cigarettes are continually promoted and perceived as a safer alternative to cigarette smoking. E-cigarettes and their modifiable nature are harmful, as the lungs are not designed for the chronic inhalation of e-cigarette vapor. It is of interest that e-cigarettes have been shown to be of no help with smoking cessation. A true danger lies in vaping, which, if ignored, will lead to disastrous future costs.


2011 ◽  
Vol 15 (4) ◽  
pp. 185-191 ◽  
Author(s):  
Lyn C. Guenther ◽  
Charles W. Lynde

Background: Herpes zoster (HZ) and postherpetic neuralgia (PHN) have a significant impact on quality of life. PHN is often chronic and difficult to treat. Dermatologists have always been involved in making the diagnosis of these conditions and, most recently, teaching the need for early antiviral therapy. Objective: With the introduction of a new vaccine, HZ and its difficult-to-treat complication PHN can be prevented or minimized. Preventive medicine is important and has been supported by dermatologists with sun safety programs. Patients receiving biologics are at increased risk of developing zoster. Conclusion: Dermatologists should embrace zoster vaccination and recommend routine vaccination of immunocompetent individuals > age 60 years, as well as patients of any age who are starting immunosuppressants, including biologics. Given that individuals over age 50 years are at risk for PHN and studies have shown that the vaccine's immunogenicity and safety are maintained in individuals age 50 to 59 years, vaccination in this age group may be considered. Some dermatologists may consider vaccinating their own patients, but most will likely recommend that vaccination be performed by their patients' primary care physicians.


2008 ◽  
Vol 294 (1) ◽  
pp. F62-F72 ◽  
Author(s):  
Daisuke Son ◽  
Ichiro Kojima ◽  
Reiko Inagi ◽  
Makiko Matsumoto ◽  
Toshiro Fujita ◽  
...  

Accumulating evidence suggests a pathogenic role of chronic hypoxia in various kidney diseases. Chronic hypoxia in the kidney was induced by unilateral renal artery stenosis, followed 7 days later by observation of tubulointerstitial injury. Proteomic analysis of the hypoxic kidney found various altered proteins. Increased proteins included lipocortin-5, calgizzarin, ezrin, and transferrin, whereas the decreased proteins were α2u-globulin PGCL1, eukaryotic translation elongation factor 1α2, and Cu/Zn superoxide dismutase (SOD1). Among these proteins, we focused on Cu/Zn-SOD, a crucial antioxidant. Western blot analysis and real-time quantitative PCR analysis confirmed the downregulation of Cu/Zn-SOD in the chronic hypoxic kidney. Furthermore, our laser capture microdissection system showed that the expression of Cu/Zn-SOD was predominant in the tubulointerstitium and was decreased by chronic hypoxia. The tubulointerstitial injury estimated by histology and immunohistochemical markers was ameliorated by tempol, a SOD mimetic. This amelioration was associated with a decrease in levels of the oxidative stress markers 4-hydroxyl-2-nonenal and nitrotyrosine. Our in vitro studies utilizing cultured tubular cells revealed a role of TNF-α in downregulation of Cu/Zn-SOD. Since the administration of anti-TNF-α antibody ameliorated Cu/Zn-SOD suppression, TNF-α seems to be one of the suppressants of Cu/Zn-SOD. In conclusion, our proteomic analysis revealed a decrease in Cu/Zn-SOD, at least partly by TNF-α, in the chronic hypoxic kidney. This study, for the first time, uncovered maladaptive suppression of Cu/Zn-SOD as a mediator of a vicious cycle of oxidative stress and subsequent renal injury induced by chronic hypoxia.


2021 ◽  
Vol 12 ◽  
Author(s):  
Shu-Hong Wang ◽  
Xue-Yu Chen ◽  
Xiao-Ping Wang

Background: Restless legs syndrome (RLS) is a common neurological disorder with unpleasant leg sensations and serious negative effects on mental and physical health. Many observational studies showed that people with RLS had a high risk of vascular diseases, including cerebrovascular and cardiovascular diseases (CVD), but the findings were conflicting. The Jidong RLS Cohort Study is a prospective cohort study designed to mainly examine whether or not RLS is associated with an increased risk of CVD.Methods and Design: The study recruited 8,867 healthy participants older than 18 years from October 2014 to December 2015. Participants received a physical examination in the Staff Hospital, Jidong Oilfield Branch, China National Petroleum Corporation. Baseline data and blood samples were collected. Restless legs syndrome was assessed using the international RLS diagnostic criteria. All of subjects would be followed up until December 2025. Major cardiovascular/cerebrovascular events including cardiac death, myocardial infarction, ischemic heart disease, heart failure, atrial fibrillation, ischemic, and hemorrhagic stroke will be the primary outcomes. Secondary outcomes include all-cause mortality, the decline in quality of life, cognitive impairment, and depression.Discussion: This study will contribute to the scientific evidence on the association between RLS and cardiovascular risks and also provide an unprecedented opportunity for early detection and prevention of CVD.


2021 ◽  
Vol 11 ◽  
Author(s):  
Chiara Tommasi ◽  
Benedetta Pellegrino ◽  
Daniela Boggiani ◽  
Angelica Sikokis ◽  
Maria Michiara ◽  
...  

Women with pathogenic germline mutations in BRCA1 and BRCA2 genes have an increased risk to develop breast and ovarian cancer. There is, however, a high interpersonal variability in the modality and timing of tumor onset in those subjects, thus suggesting a potential role of other individual’s genetic, epigenetic, and environmental risk factors in modulating the penetrance of BRCA mutations. MicroRNAs (miRNAs) are small noncoding RNAs that can modulate the expression of several genes involved in cancer initiation and progression. MiRNAs are dysregulated at all stages of breast cancer and although they are accessible and evaluable, a standardized method for miRNA assessment is needed to ensure comparable data analysis and accuracy of results. The aim of this review was to highlight the role of miRNAs as potential biological markers for BRCA mutation carriers. In particular, biological and clinical implications of a link between lifestyle and nutritional modifiable factors, miRNA expression and germline BRCA1 and BRCA2 mutations are discussed with the knowledge of the best available scientific evidence.


2016 ◽  
Vol 157 (45) ◽  
pp. 1781-1785 ◽  
Author(s):  
Iván Péter ◽  
Anna Jagicza ◽  
Zénó Ajtay ◽  
István Kiss ◽  
Balázs Németh

Psoriasis is among the most common dermatological diseases worldwide. Its significance is emphasized by adverse effects on quality of life, caused by chronic pain, physical and psychical disability due to psoriatic plaques. Besides the development of psoriatic arthritis, which often causes permanent joint damage, former studies revealed an increased risk of inflammatory bowel disease, cardiovascular disease and certain types of cancer. Genetic predisposition and oxidative stress caused by exogenous and endogenous factors can contribute to abnormal differentiation and hyperproliferation of keratinocytes, accordingly the development and maintenance of psoriasis. Moreover, excessive oxidative stress can be responsible for the onset of psoriasis complications. After a brief pathophysiological summary the authors discuss the role of oxidative stress in the development of psoriasis and its complications through several well studied biomarkers (asymmetric dimethylarginine, malondialdehyde, superoxide dismutase, catalase). Orv. Hetil., 2016, 157(45), 1781–1785.


2020 ◽  
Vol 11 ◽  
Author(s):  
Rossana Franzin ◽  
Alessandra Stasi ◽  
Marco Fiorentino ◽  
Giovanni Stallone ◽  
Vincenzo Cantaluppi ◽  
...  

The aberrant activation of complement system in several kidney diseases suggests that this pillar of innate immunity has a critical role in the pathophysiology of renal damage of different etiologies. A growing body of experimental evidence indicates that complement activation contributes to the pathogenesis of acute kidney injury (AKI) such as delayed graft function (DGF) in transplant patients. AKI is characterized by the rapid loss of the kidney’s excretory function and is a complex syndrome currently lacking a specific medical treatment to arrest or attenuate progression in chronic kidney disease (CKD). Recent evidence suggests that independently from the initial trigger (i.e., sepsis or ischemia/reperfusions injury), an episode of AKI is strongly associated with an increased risk of subsequent CKD. The AKI-to-CKD transition may involve a wide range of mechanisms including scar-forming myofibroblasts generated from different sources, microvascular rarefaction, mitochondrial dysfunction, or cell cycle arrest by the involvement of epigenetic, gene, and protein alterations leading to common final signaling pathways [i.e., transforming growth factor beta (TGF-β), p16ink4a, Wnt/β-catenin pathway] involved in renal aging. Research in recent years has revealed that several stressors or complications such as rejection after renal transplantation can lead to accelerated renal aging with detrimental effects with the establishment of chronic proinflammatory cellular phenotypes within the kidney. Despite a greater understanding of these mechanisms, the role of complement system in the context of the AKI-to-CKD transition and renal inflammaging is still poorly explored. The purpose of this review is to summarize recent findings describing the role of complement in AKI-to-CKD transition. We will also address how and when complement inhibitors might be used to prevent AKI and CKD progression, therefore improving graft function.


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