Cancer is a leading cause of death worldwide, and its incidence is continually increasing. Although anticancer therapy has improved significantly, it still has limited efficacy for tumor eradication and is highly toxic to healthy cells. Thus, novel therapeutic strategies to improve chemotherapy, radiotherapy and targeted therapy are an important goal in cancer research. Macroautophagy (herein referred to as autophagy) is a conserved lysosomal degradation pathway for the intracellular recycling of macromolecules and clearance of damaged organelles and misfolded proteins to ensure cellular homeostasis. Dysfunctional autophagy contributes to many diseases, including cancer. Autophagy can suppress or promote tumors depending on the developmental stage and tumor type, and modulating autophagy for cancer treatment is an interesting therapeutic approach currently under intense investigation. Nutritional restriction is a promising protocol to modulate autophagy and enhance the efficacy of anticancer therapies while protecting normal cells. Here, the description and role of autophagy in tumorigenesis will be summarized. Moreover, the possibility of using fasting as an adjuvant therapy for cancer treatment, as well as the molecular mechanisms underlying this approach, will be presented.

Calcium (Ca2+) homeostasis is essential for cell maintenance since this ion participates in many physiological processes. For example, the spatial and temporal organization of Ca2+ signaling in the central nervous system is fundamental for neurotransmission, where local changes in cytosolic Ca2+ concentration are needed to transmit information from neuron to neuron, between neurons and glia, and even regulating local blood flow according to the required activity. However, under pathological conditions, Ca2+ homeostasis is altered, with increased cytoplasmic Ca2+ concentrations leading to the activation of proteases, lipases, and nucleases. This review aimed to highlight the role of Ca2+ signaling in neurodegenerative disease-related apoptosis, where the regulation of intracellular Ca2+ homeostasis depends on coordinated interactions between the endoplasmic reticulum, mitochondria, and lysosomes, as well as specific transport mechanisms. In neurodegenerative diseases, alterations-increased oxidative stress, energy metabolism alterations, and protein aggregation have been identified. The aggregation of α-synuclein, β-amyloid peptide (Aβ), and huntingtin all adversely affect Ca2+ homeostasis. Due to the mounting evidence for the relevance of Ca2+ signaling in neuroprotection, we would focus on the expression and function of Ca2+ signaling-related proteins, in terms of the effects on autophagy regulation and the onset and progression of neurodegenerative diseases.

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This study evaluated biokinetic behavior of radioiodine in the bodies of ten female adult patients, with well-differentiated thyroid cancer, treated with 131I post-near total thyroidectomy, for ablation of remnant thyroid. In vivo and in vitro bioassay analyses were performed from the first hour following radioiodine administration until minimum detection limits were reached. The retention of 131I in the body from day 1 to day 6 after the intake may be mathematically represented by an exponential decreasing curve, with an average biological half-life of approximately 0.81 d, with the exception of patients who presented thyroiditis. From day 6 to day 13, urinary excretion rates indicated an increased liberation of iodine. After 2 wk, the body retention of iodine followed an exponential decrease, with a half-life of about 15 d. The average whole-body dose for these patients was 0.27 Gy, as estimated through cytogenetic techniques.

Agradeço a minha mãe Ivonete por sempre estar ao meu lado, me incentivando e apoiando e sendo sempre o meu porto seguro. Ao meu irmão Claigton que se tornou o meu braço direito, e me fez descobrir que sempre podemos ver o lado positivo das coisas. Aos meus filhos, Davi e Anabel, por serem o colorido da minha vida e a minha inspiração para sempre buscar o melhor. À minha tia Bete que foi uma segunda mãe, me amparando nos momentos que mais precisei. Ao professor Marco Aurélio Cremasco pela oportunidade concedida para realização do doutorado, pela paciência e pela orientação. Obrigada por todo o cuidado e apoio durante todos esses anos!