Mirna Stela Stela Ludwig

By Thiago Gomes Heck, Sofia Pizzato Scomazzon, Mirna Stela Ludwig and Paulo Ivo Homem de Bittencourt Jr.

Part of the book: Skeletal Muscle

By Thiago Gomes Heck, Mirna Stela Ludwig, Analu Bender dos Santos and Pauline Brendler Goettems-Fiorin

This chapter discusses about subclinical processes related to insulin resistance development that worsen the muscle metabolic functions, generated by factors such as lifestyle (bad quality food intake and sedentary behavior) and aging. Also discussed are the effects of regular physical exercise as a strategy to prevent the metabolic impairment in organisms, approaching since muscle subclinical molecular processes to the whole body’s integrative physiology. Insulin resistance development includes modification in the pattern of inflammatory cytokines, heat shock proteins, tissue- specific defects in insulin action and signaling, oxidative stress and ectopic lipid deposition. The exercise is a known modulator of all parameters listed above and has important role in the regulation of “immune-metabolic” homeostasis from the muscle to the whole body. This chapter aims to present a new molecular approach related to the control of metabolism and encourage scientists and students to propose new strategies against insulin resistance and diabetes type 2 developments.

Part of the book: Muscle Cell and Tissue

By Thiago Gomes Heck, Pauline Brendler Goettems Fiorin, Matias Nunes Frizzo and Mirna Stela Ludwig

Epidemiologic and experimental studies suggest that environmental exposures to air pollutants can increase prevalence of metabolic and cardiorespiratory diseases. Among the risk factors, many studies have shown that air pollution, especially by fine particulate matter (PM2.5), can lead to the development of type 2 diabetes mellitus (T2DM) or make diabetics more susceptible to other health complications. This chapter aimed to discuss the pathophysiologic mechanisms evolved in susceptibility to cardiorespiratory PM2.5 effects in T2DM subjects, as well as the enhancing effect of PM2.5 exposure on development of T2DM. We discussed the pathophysiologic mechanisms of PM2.5 exposure and T2DM based on pro−/anti-inflammatory balance, metabolic regulation, redox status, and heat shock response, reinforcing the complex nature of T2DM etiology and highlighting the PM2.5 air pollution as a critical health problem.

Part of the book: Diabetes and Its Complications

By Pauline Brendler Goettems Fiorin, Mirna Stela Ludwig, Matias Nunes Frizzo and Thiago Gomes Heck

Particulate matter (PM) is a mixture of solid particles and liquid droplets found in the air, and it is one of the most harmful air pollutants. When inhaled, it affects the pulmonary system, cardiovascular systems, and other tissues. The size, composition, and deposition of PM, mainly related to fine and ultrafine particulate matter, are factors that determine the harmful effects of exposure to particles. Among the main effects is the inducer of ROS production, and consequently oxidative tissue damage in target organs and other responses, mediated by inflammatory cytokines and cellular stress response. The main pathway through which particles are potent mediators of oxidative stress is the damage caused to DNA and lipid molecules, whereas the pro-inflammatory response involves an immune response against PM, which in turn, it is related to cell stress responses observed by heat shock proteins (HSPs) expression and release. Thus, the ability of an organism to respond to PM inhalation requires anti-oxidative, anti-inflammatory, and cellular stress defenses that can be impaired in susceptible subjects as people with chronic diseases as diabetes and obesity. In this chapter, we discuss the mechanistic aspects of PM effects on health and present some animal research models in particle inhalation studies.

Part of the book: Reactive Oxygen Species

By Joise Wottrich, Eduardo Gonçalves, Carina Echer de Souza, Pauline Brendler Goettems Fiorin, Mirna Stela Ludwig, Thiago Gomes Heck and Matias Nunes Frizzo

The new coronavirus first appeared in December 2019 in Wuhan, China, being officially named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) by the International Committee on Taxonomy of Viruses (ICTV), as well as the name of the disease has been described as COVID-19 (coronavirus disease 2019). In March 2020, the disease was considered a global pandemic, with currently more than 514 million cases worldwide, with 6.4 million deaths. Severe cases of COVID-19 progress to acute respiratory distress syndrome (ARDS), on average about 8–9 days after the onset of symptoms. It is also worth mentioning that the severity of the disease in patients is not only due to the viral infection but also due to the host response. This phase, called a cytokine storm, reflects a state of systemic immune activation, with high levels of cytokines, such as IL-6, IL-1b, IL-2, IL-12, IL-18, TNF, and interferon gamma (IFN-γ). In this sense, the management of the disease largely depends on symptomatic and supportive treatments. For severely or critically ill patients with acute respiratory distress syndrome (ARDS) and sepsis, in addition to supplemental oxygen, mechanical ventilation, and ARDS-specific therapies, antiviral and antibiotic treatments should also be considered. Thus, the purpose of this chapter is to describe the pathophysiology and treatment of SARS-CoV-2 infection.

Part of the book: COVID-19 Drug Development

By Eduardo Almeida de Souza Minuzzo, Pauline Brendler Goettems Fiorin, Vítor Antunes de Oliveira, Mirna Stela Ludwig and Matias Nunes Frizzo

The Intensive Care Unit (ICU) has the highest incidence of patients with various infectious processes. Sepsis, a systemic inflammatory response syndrome associated with infections, is characterized by inflammatory cytokine production, innate immune system activation, mitochondrial damage, and severe organ dysfunction. Early diagnosis is crucial for appropriate therapeutic interventions and reducing mortality. Various biomarkers have been studied for diagnostic and prognostic purposes, including lactate, interleukins, C-reactive protein, and procalcitonin. Immune-inflammatory biomarkers, such as leukogram, leukocyte ratios, neutrophil variation index, and leukocyte morphological parameters, provide valuable information about sepsis severity and progression. Additionally, redox state and cellular stress response biomarkers contribute to understanding sepsis pathophysiology and organ dysfunction stratification. The combined use of these biomarkers allows for more accurate diagnoses, early treatment, reduced hospital stays, minimized sequelae, and decreased sepsis mortality risk. This chapter describes the applicability of clinical and laboratory parameters as biomarkers for diagnosing and prognosing infectious processes and sepsis in ICU patients.

Part of the book: Septic Shock