Temporal Trend of the Prevalence of Modifiable Risk Factors of Stroke: An Ecological Study of Brazilians between 2006 and 2012.

Stroke is one of the leading causes of death worldwide, including in Brazil. This study aimed to analyze the temporal trend of the prevalence of modifiable risk factors of stroke from 2006 to 2012. This ecological study was conducted by secondary analysis in May 2018, using data from the surveillance of risk factors and protection for chronic diseases by telephone inquiry (VIGITEL) available in the Department of Informatics of the Unified Health System (DATASUS). The modifiable risk factors of stroke in Brazilians were systemic arterial hypertension, diabetes mellitus, abusive alcohol consumption, overweight, and obesity. Overall, there was a significant increase in the risk factors of diabetes (ß = 0.30, P = 0.001, r2 = 0.99), overweight (ß = 0.50, P = 0.002, r2 = 0.98), and obesity (ß = 0.88, P < 0.001, r2 = 0.96). However, there was a stability in the prevalence of hypertension (ß = 0.25, P = 0.320, r2 = 0.88) and alcohol abuse (ß = 0.32, P = 0.116, r2 = 0.49). There was an increase in the prevalence of diabetes mellitus, overweight, and obesity, but stability in systemic arterial hypertension and abusive alcohol consumption in the Brazilian population.

Reduction on Proinflammatory Cytokines after Application of Transcutaneous Electrical Nerve Stimulation (TENS) in Patients with a Breast Cancer: A Nonrandomized, Open, and Single-Arm Study Protocol with Paired Analysis.

BACKGROUND: Transcutaneous electrical nerve stimulation (TENS) has been used as analgesic therapy in many diseases. It is already known that studies that have observed the relationship between pain and cytokines have found that patients who report less severe pain have less production of proinflammatory cytokines. However, one another accepted mechanism is that decreasing proinflammatory cytokines results in decreased pain intensity. Analyzing the literature, the authors describe that, in addition to the analgesic effect, TENS has shown systemic effects, and clinically, the reduction of proinflammatory cytokines could be a protective factor against inflammation. To test the inflammatory effect of TENS, we researched the literature for clinical conditions that suggest that proinflammatory cytokines are one of the main mediators of the disease process. Chronic inflammation is one of the risk factors mentioned for the development of a new cancer; at the same time, it is indicated as an indicator of the worst prognosis. Studies also suggest that the worst prognosis of breast cancer, one of the types with the highest incidence in the world, may be related to increased inflammatory activity. Considering that inflammation is increased in breast cancer and that TENS can reduce proinflammatory cytokines even without blocking the pain pathway, our hypothesis is that the anti-inflammatory effect of TENS can bring benefits to these patients. The aim of this study will be to evaluate the effect of TENS on blood reduction of proinflammatory cytokines in breast cancer patients. METHODS: This study will evaluate at least 59 patients, over 18 years of age, diagnosed with breast cancer, but who have not yet started any treatment. All patients will be submitted to TENS intervention (Ibramed, Model Neurodyn III, parameters: VIF-turn on, frequency-2-247 Hz, pulse size-50-500 µs, and intensity (mA)-maximum tolerated by the patient), and the data will be analyzed in the pre- and postintervention of each patient. The application has a total duration of 30 minutes, and 8 ml of blood will be collected before and after the intervention. Proinflammatory (IL-1, IL-2, IL-6, IL-7, and TNF-α) and anti-inflammatory (IL-4, IL-10, IL-13, and FTCß) cytokines will be analyzed. As a primary endpoint, we will analyze the reduction in blood concentration of proinflammatory cytokines, and as secondary endpoints, we will analyze the size of the effect according to each type of proinflammatory cytokine, describe the effect size of the reduction according to the breast cancer immunohistochemistry, and analyze the effect of TENS on anti-inflammatory cytokines. This study is approved by the Research Ethics Committee (Centro Universitário FMABC, Brazil) and registered in the Brazilian Clinical Trials (Search text: RBR-10jbwh47).

Noncoding RNAs and Colorectal Cancer: A General Overview.

Colorectal cancer (CRC) is the second most prevalent cancer in the world in which nonmelanoma skin cases are not considered. Different epigenetic mechanisms play a role in the development of cancer. Noncoding RNAs (ncRNAs) are RNA molecules transcribed from noncoding regions of the genome. These are divided into sncRNAs (small noncoding RNAs: <200 nucleotides - including miRNAs [microRNAs], siRNAs [small interfering RNAs], piRNAs [piwi-interacting RNAs], snoRNAs [small nucleolar RNAs]) and lncRNAs (long noncoding RNAs: >200 nucleotides - includingcircular RNAs [circRNAs]). NcRNAs can act as oncogenes or as tumor suppressor genes in CRC and are potential biomarkers of diagnosis, with possible clinical implications. This article aims to conduct a general review of all types of non-coding RNAs and their influence in colorectal cancer, focus on biomarkers of CRC and their possible applications in clinical practice, as well as review their biogenesis and functions. Furthermore, we seek to summarize possible databases available for new searches and studies that require sequence annotation, comparison sequences and target prediction for ncRNAs with the hope of gathering information that can aid in the process of understanding and translating the use of ncRNAs into clinical practice.

Evaluation of the impact of single-nucleotide polymorphisms on treatment response, survival and toxicity with cytarabine and anthracyclines in patients with acute myeloid leukaemia: a systematic review protocol.

INTRODUCTION: Acute myeloid leukaemia is the most common type of acute leukaemia in the world. Thus, the study of genetic alterations, such as single-nucleotide polymorphisms (SNPs), has contributed to a better understanding of the mechanisms underlying leukaemogenesis, to improve the prognosis and to increase the survival of these patients. However, there is no synthesis of evidence in the literature evaluating the quality of evidence and the risk of bias in the studies such that the results can be translated. Thus, this systematic review protocol aims to assess the impact of SNPs on genes involved in the metabolism of cytarabine and anthracyclines with respect to survival, treatment response and toxicity in patients with AML. METHODS: This systematic review protocol is based on PRISMA guidelines and includes searches in six electronic databases, contact with authors, repositories of clinical trials, and cancer research. Studies published in peer-reviewed journals will be included if they meet the eligibility criteria: (a) samples composed of individuals of any age, of both sexes, with a diagnosis of AML, regardless of the time of diagnosis of disease; (b) participants who have undergone or are undergoing cytarabine- and anthracycline-associated chemotherapy or cytarabine-only chemotherapy; and (c) in vivo studies. Studies that include patients with promyelocytic leukaemia (Fab type 3) will be excluded because this disease has different treatment. The process of study selection, data extraction, and evaluation/synthesis will be performed in duplicate. Assessment of methodological quality and risk of bias will be performed using the Cochrane Risk of Bias Tool for randomized clinical studies and the Downs-Black Checklist for cohort and case-control studies. The synthesis of evidence will include the level of evidence based on the GRADE protocol. A meta-analysis of the association between SNPs and outcomes may be performed based on Cochrane guidelines. DISCUSSION: It is expected that clinical decisions for AML patients will consider evidence-based practices to contribute to better patient management. In this way, we will be able to define how to treat patients with AML to improve their survival and quality of life. SYSTEMATIC REVIEW REGISTRATION: PROSPERO CRD42018100750.