scholarly journals The Link between Obesity, Microbiota Dysbiosis, and Neurodegenerative Pathogenesis

Diseases ◽  
2021 ◽  
Vol 9 (3) ◽  
pp. 45
Author(s):  
Emanuel Vamanu ◽  
Sachchida Nand Rai
Keyword(s):  
Molecular Mechanisms ◽  
Degenerative Diseases ◽  
Microbial Dysbiosis ◽  
Physicochemical Factors ◽  
The World ◽  
Inflammatory Processes ◽  
Prevalence Of Obesity ◽  
Molecular Aspects ◽  
Major Factors

Current research in medicine in several parts of the world has attempted to establish a link between the occurrence of neurodegenerative pathologies, microbiota dysbiosis, and the incidence of obesity. The body’s response to different physicochemical factors has also been influenced by the proper assimilation of bioactive compounds contained in the food that is ingested. Oxidative stress is one of the major factors that directly affects the functioning of the human microbiota. The body’s reaction to this imbalance is crucial to the progression of inflammatory processes, which are based on molecular mechanisms. Microbial dysbiosis can result in a possibly permanent alteration in the physiological response. This review aims to highlight recent contributions made to alleviating human dysbiosis in degenerative diseases, especially for neurodegenerative pathologies based on the rising prevalence of obesity. We discuss the significance of both microbiota modulation and possible alleviations of pathologies by a modulatory function. We argue that pre- and probiotics (including phenolic compounds stimulating the favorable strain from the microbiota) are an effective alternative that can support the microbiota pattern’s modulation over time and the attenuation of indirect causes that determine dysbiosis. Molecular aspects are presented in support of the modulating role of the microbiota following the use of probiotics.

scholarly journals THIOZOLIDINEDIONES IN THE TREATMENT OF PATIENTS WITH EXTENSIVE PSORIASIS AND CONCOMITANT ALIMENTARY OBESITY

2020 ◽  
Vol 20 (4) ◽  
pp. 30-34
Author(s):  
Ya.O. Yemchenko ◽  
K.Ye. Ishcheikin ◽  
I.P. Kaidashev
Keyword(s):  
Systemic Inflammation ◽  
Molecular Mechanisms ◽  
Current Data ◽  
The Body ◽  
Internal Organs ◽  
Single View ◽  
Multifactorial Diseases ◽  
Alimentary Obesity ◽  
Inflammatory Processes

Psoriasis is one of the most common chronic recurrent systemic autoimmune multifactorial diseases, affected the skin, joints, internal organs and systems of the body. Despite the significant prevalence of psoriasis and a large number of studies devoted this problem there is still no single view on the pathogenesis of this dermatosis. To clear up the pathogenesis of psoriasis, it seems to be reasonable to focus on the common comorbidities or multimorbidities, which may occur in the course of psoriasis, as this issue is still insufficiently studied. Recent reports have proven the evidences of indisputable link between psoriasis and obesity. The scientific literature extensively covers the issues of identical pathogenetic mechanisms of inflammatory processes in psoriasis and obesity. Given the current data on the role of systemic inflammation underlying the development of both psoriasis and obesity, the study of molecular mechanisms of its development and in particularly the role of proinflammatory nuclear transcription factors, thiazolidinediones have been found out as pathogenetically justified medicine of choice for the therapy of these diseases. In this study, we determined the effectiveness of using 30 mg of pioglitazone daily for 6 months in the course of treatment for patients with extensive psoriasis vulgaris of moderate severity, who were also diagnosed as having concomitant grade І-ІІ alimentary obesity that was supported by clinical and immunological findings evidenced of systemic inflammation. Analyzing the results obtained, we have found out the prolonged therapy with pioglitazone leads to a decrease in systemic inflammation and contributes to a milder recurrent course of psoriasis.

Cancer epidemiology and public health

2021 ◽  
pp. 17-42
Author(s):  
Paolo Boffetta ◽  
Zuo-Feng Zhang ◽  
Carlo La Vecchia
Keyword(s):  
Public Health ◽  
Risk Factors ◽  
Molecular Mechanisms ◽  
Cancer Epidemiology ◽  
Attributable Risk ◽  
World Population ◽  
The World ◽  
Near Future ◽  
Epidemiology And Public Health

Neoplasms continue to dominate globally as one of the major sources of human disease and death. There are multiple modifiable causes of cancer and understanding their attributable risk factors for each cancer is of importance. This chapter covers the role of cellular and molecular mechanisms as well as the experimental and epidemiological approaches as determinants of the main cancers. Even if major discoveries in the clinical management of cancer patients will be accomplished in the near future, the changes will mainly affect the affluent part of the world population. Promising approaches focused on prevention of the known causes, reducing its consequences, notably in resource-constrained settings are highlighted.

Molecular Interactions of α-Synuclein, Mitochondria, and Cellular Degradation Pathways in Parkinson's Disease

2020 ◽  
pp. 212-234
Author(s):  
Mansi Verma ◽  
Sujata Basu ◽  
Manisha Singh ◽  
Rachana R. ◽  
Simrat Kaur ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Molecular Interactions ◽  
Therapeutic Target ◽  
Molecular Mechanisms ◽  
Degradation Pathways ◽  
Functional Changes ◽  
The World ◽  
Novel Therapeutic

Parkinson's disease (PD) has been reported to be the most common neurodegenerative diseases all over the world. Several proteins are associated and responsible for causing PD. One such protein is α-synuclein. This chapter discusses the role of α-synuclein in PD. Various genetic and epigenetic factors, which cause structural and functional changes for α-synuclein, have been described. Several molecular mechanisms, which are involved in regulating mitochondrial and lysosomal related pathways and are linked to α-synuclein, have been discussed in detail. The knowledge gathered is further discussed in terms of using α-synuclein as a diagnostic marker for PD and as a novel therapeutic target for the same.

Molecular signatures of Emery–Dreifuss muscular dystrophy

2008 ◽  
Vol 36 (6) ◽  
pp. 1354-1358 ◽  
Author(s):  
Matthew A. Wheeler ◽  
Juliet A. Ellis
Keyword(s):  
Muscular Dystrophy ◽  
Dilated Cardiomyopathy ◽  
Molecular Mechanisms ◽  
Autosomal Dominant ◽  
Signalling Pathways ◽  
Lamin A ◽  
Degenerative Diseases ◽  
Hypertrophic Growth ◽  
Genes Encoding

Mutations in genes encoding the nuclear envelope proteins emerin and lamin A/C lead to a range of tissue-specific degenerative diseases. These include dilated cardiomyopathy, limb-girdle muscular dystrophy and X-linked and autosomal dominant EDMD (Emery–Dreifuss muscular dystrophy). The molecular mechanisms underlying these disorders are poorly understood; however, recent work using animal models has identified a number of signalling pathways that are altered in response to the deletion of either emerin or lamin A/C or expression of Lmna mutants found in patients with laminopathies. A distinguishing feature of patients with EDMD is the association of a dilated cardiomyopathy with conduction defects. In the present article, we describe several of the pathways altered in response to an EDMD phenotype, which are known to be key mediators of hypertrophic growth, and focus on a possible role of an emerin–β-catenin interaction in the pathogenesis of this disease.

scholarly journals Cellular Responses to Proteasome Inhibition: Molecular Mechanisms and Beyond

2019 ◽  
Vol 20 (14) ◽  
pp. 3379 ◽  
Author(s):  
Nicolas Albornoz ◽  
Hianara Bustamante ◽  
Andrea Soza ◽  
Patricia Burgos
Keyword(s):  
Side Effects ◽  
Inclusion Bodies ◽  
Molecular Mechanisms ◽  
Proteasome Inhibitors ◽  
Proteasome Inhibition ◽  
Cellular Responses ◽  
Cell Responses ◽  
Different Types ◽  
Inflammatory Processes

Proteasome inhibitors have been actively tested as potential anticancer drugs and in the treatment of inflammatory and autoimmune diseases. Unfortunately, cells adapt to survive in the presence of proteasome inhibitors activating a variety of cell responses that explain why these therapies have not fulfilled their expected results. In addition, all proteasome inhibitors tested and approved by the FDA have caused a variety of side effects in humans. Here, we describe the different types of proteasome complexes found within cells and the variety of regulators proteins that can modulate their activities, including those that are upregulated in the context of inflammatory processes. We also summarize the adaptive cellular responses activated during proteasome inhibition with special emphasis on the activation of the Autophagic-Lysosomal Pathway (ALP), proteaphagy, p62/SQSTM1 enriched-inclusion bodies, and proteasome biogenesis dependent on Nrf1 and Nrf2 transcription factors. Moreover, we discuss the role of IRE1 and PERK sensors in ALP activation during ER stress and the involvement of two deubiquitinases, Rpn11 and USP14, in these processes. Finally, we discuss the aspects that should be currently considered in the development of novel strategies that use proteasome activity as a therapeutic target for the treatment of human diseases.

scholarly journals Molecular Mechanisms Underlying the Relationship between Obesity and Male Infertility

Metabolites ◽  
2021 ◽  
Vol 11 (12) ◽  
pp. 840
Author(s):  
Federica Barbagallo ◽  
Rosita A. Condorelli ◽  
Laura M. Mongioì ◽  
Rossella Cannarella ◽  
Laura Cimino ◽  
...  
Keyword(s):  
Male Infertility ◽  
Molecular Mechanisms ◽  
Premature Mortality ◽  
Male Reproduction ◽  
Increased Risk ◽  
Inflammatory Processes ◽  
Prevalence Of Obesity ◽  
Treatment Of Obesity ◽  
The Relationship ◽  
And Oxidative Stress

In recent decades, the worldwide prevalence of obesity has risen dramatically and is currently estimated to be around 20%. Obesity is linked to an increased risk of comorbidities and premature mortality. Several studies have shown that obesity negatively impacts male fertility through various mechanisms. This review aims to investigate the molecular mechanisms through which obesity impairs male reproduction, including obesity-associated hypogonadism and its effects on spermatogenesis, chronic inflammation, and oxidative stress. Obesity negatively impacts both conventional and biofunctional sperm parameters, and it also induces epigenetic changes that can be transferred to offspring. Moreover, obesity-related diseases are linked to a dysregulation of adipocyte function and micro-environmental inflammatory processes. The dysregulated adipokines significantly influence insulin signaling, and they may also have a detrimental effect on testicular function. Sirtuins can also play an important role in inflammatory and metabolic responses in obese patients. Understanding the molecular mechanisms that are involved in obesity-induced male infertility could increase our ability to identify novel targets for the prevention and treatment of obesity and its related consequences.

scholarly journals Role of IL-33/ST2 Axis in Chronic Inflammatory Neurological Disorderss

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Jelena Dimitrijevic ◽  
Aleksandar Arsenijevic ◽  
Marija Milovanovic ◽  
Bojana Stojanovic ◽  
Dragana Arsenijevic ◽  
...  
Keyword(s):  
Immune Responses ◽  
Tissue Repair ◽  
Degenerative Diseases ◽  
Cell Necrosis ◽  
Dual Roles ◽  
Interleukin 33 ◽  
Biological Features ◽  
Inflammatory Processes ◽  
The Central Nervous System

Abstract Interleukin-33 (IL-33) is a member of IL-1 family of cytokines, produced constitutively by fibroblasts, endothelial cells, and epithelial cells. IL-33 can be released passively from cells during tissue damage and cell necrosis, suggesting that it may act as an alarmin. Function of IL-33 is mediated by its interaction with ST2 molecule that is expressed on many immune cells: Th2 lymphocytes, NK, NKT and mast cells, monocytes, dendritic cells and granulocytes. IL-33/ST2 pathway plays, often dual, roles in different physiological and inflammatory processes, mediating both, pathological immune responses and tissue repair. Expression of IL-33 in the central nervous system (CNS) is significantly enhanced during various pathological processes, indicating its important role in the pathogenesis of neurological inflammatory and degenerative diseases. In this review the biological features, expression of IL-33 and its ligand ST2 in CNS, and the role of IL- 33/ST2 pathway in development of Alzheimer’s disease and multiple sclerosis are discussed.

Role of DNA damage and repair mechanisms in uterine fibroid/leiomyomas: a review

2020 ◽  
Author(s):  
Sneh M Toprani ◽  
Varsha Kelkar Mane
Keyword(s):  
Dna Damage ◽  
Molecular Mechanisms ◽  
Healthcare Sector ◽  
Clinical Aspects ◽  
Dna Damage And Repair ◽  
Myometrial Cells ◽  
Mutational Burden ◽  
The World ◽  
Repair Mechanisms

Abstract There has been a significant annual increase in the number of cases of uterine leiomyomas or fibroids (UF) among women of all races and ages across the world. A fortune is usually spent by the healthcare sector for fibroid-related treatments and management. Molecular studies have established the higher mutational heterogeneity in UF as compared to normal myometrial cells. The contribution of DNA damage and defects in repair responses further increases the mutational burden on the cells. This in turn leads to genetic instability, associated with cancer risk and other adverse reproductive health outcomes. Such and many more growing bodies of literature have highlighted the genetic/molecular, biochemical and clinical aspects of UF; none the less there appear to be a lacuna bridging the bench to bed gap in addressing and preventing this disease. Presented here is an exhaustive review of not only the molecular mechanisms underlying the predisposition to the disease but also possible strategies to effectively diagnose, prevent, manage, and treat this disease.

Exploring the role of website quality and hedonism in the formation of e-satisfaction and e-loyalty

2017 ◽  
Vol 11 (3) ◽  
pp. 246-267 ◽  
Author(s):  
Asad Ahmad ◽  
Obaidur Rahman ◽  
Mohammed Naved Khan
Keyword(s):  
Factor Analysis ◽  
Customer Service ◽  
Structural Equation ◽  
World Market ◽  
Content Type ◽  
Internet Users ◽  
Online Retailers ◽  
The World ◽  
Major Factors

Purpose The purpose of this study is to explore the factors that help in building e-loyalty towards online retailers. Internet has brought the world market into a single platform. Marketers have started using Internet as a new and innovative way to interact and reach people all around the world. With the increase in the number of Internet users, the number of e-marketers has also increased. In the context of online retailing, the service quality being offered is increasingly being used as a tool for competitive advantage. E-tailers are embracing superior e-services to attract, retain and convert patrons into loyal customers. Design/methodology/approach The researchers in the present study have used a research instrument that consists of constructs of the modified eTailQ scale, hedonism and e-satisfaction that together result in the formation of e-loyalty. Researcher-controlled sampling was employed to collect data from 159 student respondents. Findings Exploratory factor analysis, confirmatory factor analysis and structural equation modelling were applied for analysing the collected data. The results of the study demonstrate that major factors which help in the formation of e-loyalty are e-satisfaction, customer service, privacy and hedonism. Originality/value This study extends the understanding of the role of e-satisfaction, customer service, privacy and hedonism in the formation of loyal consumers. The researchers proposed a model to study the factors impacting the e-loyalty of the Internet shoppers in India. The findings of the study are expected to help both researchers and marketers.

scholarly journals Peripheral Mechanisms of Dental Pain: The Role of Substance P

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Paola Sacerdote ◽  
Luca Levrini
Keyword(s):  
Substance P ◽  
Molecular Mechanisms ◽  
Dental Pain ◽  
Therapeutic Strategies ◽  
Current Evidence ◽  
Trigeminal Ganglia ◽  
Clinical Observations ◽  
P Concentration ◽  
Inflammatory Processes

Current evidence supports the central role of neuropeptides in the molecular mechanisms underlying dental pain. In particular, substance P, a neuropeptide produced in neuron cell bodies localised in dorsal root and trigeminal ganglia, contributes to the transmission and maintenance of noxious stimuli and inflammatory processes. The major role of substance P in the onset of dental pain and inflammation is increasingly being recognised. Well-grounded experimental and clinical observations have documented an increase in substance P concentration in patients affected by caries, pulpitis, or granulomas and in those undergoing standard orthodontic or orthodontic/dental care procedures. This paper focuses on the role of substance P in the induction and maintenance of inflammation and dental pain, in order to define future lines of research for the evaluation of therapeutic strategies aimed at modulating the complex effects of this mediator in oral tissues.

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