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This paper explains the problem that DST (Departamento de Soporte Tecnico) has to face every day, this department is responsible for managing the technology resources of FIEC (Facultad de Ingenieria Electrica y Computacion) through the process of lending computers and monitoring availably of resources. The process of lending computer equipment for students defines that every incident about lost or disconnection of any computer peripheral device must be register, but it has been made manually. This paper also provides information on the implementation of a system in order to avoid peripherals theft in laboratories and to prevent damage to servers as well as by high temperatures or excess moisture.

Ill children are at risk but rarely screened for myocardial injury. The frequency of such injury in ill children is unknown. Elevated levels of plasma cardiac troponin I (cTnI) can detect subclinical myocardial injury.We measured cTnI levels from 283 Children's Hospital, Boston patients (median age 2.10 years, range 0.13-22.4 years) seen in an outpatient or emergency clinic without clinically apparent cardiac disease. We tookor = 0.5 ng/mL as an indication of myocardial injury. We also measured plasma creatine kinase-MB, total creatine kinase, and myoglobin, and performed a chart review.Fifteen (7.8%) of the 193 acutely ill children and 4 (4.4%) of the 90 well children had an elevated cTnI level (P = .44). Within the acutely ill group, the children with elevated cTnI were younger and had lower mean hemoglobin and hematocrit levels. Cardiac troponin I levels correlated with creatine kinase-MB (r = 0.22; P.001) but not with creatine kinase or myoglobin. The 4 children with cTnI0.89 ng/mL, who also had plasma cardiac troponin T measured, showed cardiac troponin T elevations that were consistent with unstable angina levels in adults. Four children had high-level cTnI elevations (2 ng/mL) consistent with acute myocardial infarction levels in adults.Elevated cTnI levels occur in children without clinically apparent cardiac disease and can be at adult unstable angina or acute myocardial infarction levels. Prospective studies to determine the clinical significance of these findings and their relationship to the development of cardiomyopathy are warranted.

Many children and adolescents with cancer receive chemotherapeutic agents that are cardiotoxic. Thus, while survival rates in this population have improved for some cancers, many survivors may experience acute or chronic cardiovascular complications that can impair their quality of life years after treatment. In addition, cardiac complications of treatment lead to reductions in dose and duration of chemotherapy regimens, potentially compromising clinical efficacy. Anthracyclines are well known for their cardiotoxicity, and alkylating agents, such as cyclophosphamide, ifosfamide, cisplatin, busulfan, and mitomycin, have also been associated with cardiotoxicity. Other agents with cardiac effects include vinca alkaloids, fluorouracil, cytarabine, amsacrine, and asparaginase and the newer agents, paclitaxel, trastuzumab, etoposide, and teniposide. The heart is relatively vulnerable to oxidative injuries from oxygen radicals generated by chemotherapy. The cardiac effects of these drugs include asymptomatic electrocardiographic abnormalities, blood pressure changes, arrhythmias, myocarditis, pericarditis, cardiac tamponade, acute myocardial infarction, cardiac failure, shock, and long-term cardiomyopathy. These effects may occur during or immediately after treatment or may not be apparent until months or years after treatment. Mild myocardiocyte injury from chemotherapy may be of more concern in children than in adults because of the need for subsequent cardiac growth to match somatic growth and because survival is longer in children. Primary prevention is therefore important. Patients should be educated about the cardiotoxic risks of treatment and the need for long-term cardiac monitoring before chemotherapy is begun. Cardiotoxicity may be prevented by screening for risk factors, monitoring for signs and symptoms during chemotherapy, and continuing follow-up that may include electrocardiographic and echocardiographic studies, angiography, and measurements of biochemical markers of myocardial injury. Secondary prevention should aim to minimize progression of left ventricular dysfunction to overt heart failure. Approaches include altering the dose, schedule, or approach to drug delivery; using analogs or new formulations with fewer or milder cardiotoxic effects; using cardioprotectants and agents that reduce oxidative stress during chemotherapy; correcting for metabolic derangements caused by chemotherapy that can potentiate the cardiotoxic effects of the drug; and cardiac monitoring during and after cancer therapy. Avoiding additional cardiotoxic regimens is also important in managing these patients. Treating the adverse cardiac effects of chemotherapy will usually be dependent on symptoms or will depend on the anticipated cardiovascular effects of each regimen. Treatments include diuresis, afterload reduction, beta-adrenoceptor antagonists, and improving myocardial contractility.

PURPOSE: A common late effect of doxorubicin therapy for childhood cancer is reduced left-ventricular (LV) wall thickness resulting in elevated LV afterload and depressed LV function. Many children are given angiotensin-converting enzyme inhibitors, which have been studied primarily in adults. We document the long-term effects of angiotensin-converting enzyme inhibitors in doxorubicin-treated survivors of childhood cancer. PATIENTS AND METHODS: In this retrospective study, we reviewed records of 18 children who had regular echocardiographic examinations during enalapril therapy (mean age at cancer diagnosis, 8 years; mean time between completion of doxorubicin therapy and start of enalapril, 7 years; median follow-up since the start of enalapril, 10 years). RESULTS: Over the first 6 years of enalapril therapy, there was progressive improvement toward normal values in LV dimension, afterload, fractional shortening, and mass, but all these parameters deteriorated between 6 and 10 years. LV wall thickness deteriorated throughout the study period, as did LV contractility and systolic blood pressure. Diastolic blood pressure fell slightly. By 6 years on enalapril, all six patients who had had congestive heart failure at the start of enalapril therapy had either died or undergone cardiac transplantation, compared with three of the 12 asymptomatic patients. CONCLUSION: In doxorubicin-treated long-term survivors of childhood cancer, enalapril-induced improvement in LV structure and function is transient. The primary defect, which is LV wall thinning, continues to deteriorate, and thus the short-term improvement was mostly related to lowered diastolic blood pressure.

The goals of care for patients at risk for cardiomyopathy induced by cancer treatment should include prevention, early diagnosis, treatment of subclinical cardiac dysfunction, prevention of disease progression, and prolongation of patient survival. Any strategy aimed to minimize the cardiotoxic effects of cancer treatment should maintain the treatment's antineoplastic efficacy. Successful therapy achieves the highest health-related quality of life that is defined by the balance between maximizing the efficacy of oncologic therapy and minimizing the toxicity of this therapy. Doxorubicin-induced cardiotoxicity can be reduced by limiting the overall cumulative dose. There is no specific treatment for cancer therapy-related cardiomyopathy, and symptomatic patients should receive standard treatments for congestive heart failure such as afterload reduction, beta-blockers, diuresis, and digoxin. Afterload reduction with angiotensin-converting enzyme inhibitors such as enalapril and captopril may be indicated in patients with elevated afterload and asymptomatic left ventricular dysfunction diagnosed by echocardiography. Beta-blockers may improve myocardial systolic dysfunction and may be useful in the treatment of cancer treatment-induced cardiomyopathy. Cardiac transplantation remains a viable option in patients with cancer treatment-induced end-stage heart disease.

Objetivou-se identificar e quantificar os constituintes e avaliar a atividade antimicrobiana dos óleos essenciais de Mentha piperita, Cymbopogon citratus, Ocimum basilicum e Origanum majorana contra cepas de Escherichia coli enteropatogênica, Salmonella enterica Enteritidis, Listeria monocytogenes e Enterobacter sakazaki. A obtenção dos óleos essenciais foi realizada a partir de folhas secas, empregando-se a técnica de hidrodestilação e utilizando-se a aparelho de Clevenger modificado. A atividade antibacteriana dos óleos essenciais foi determinada pelo método de difusão em ágar. Observou-se que os óleos essenciais inibiram o crescimento bacteriano, mas a efetividade foi variada. Entre os óleos essenciais testados, M. piperita apresentou maior atividade antibacteriana para E. coli, (8.106 UA mL-1) quando comparada as demais bactérias, atividade moderada para Salmonella enterica Enteritidis e Enterobacter sakazakii (1.706 e 3.200 UA mL-1 respectivamente) e baixa atividade para Listeria monocytogenes (106,67 UA mL-1). Já óleo essencial de Cymbopogon citratus apresentou maior atividade antimicrobiana frente a E. coli (9.386 UA mL-1) e atividade moderada frente a Enterobacter sakazakii, Salmonella enterica Enteritidis e Listeria monocytogenes (2.773 UA mL-1 para ambas). Ocimum basilicum apresentou maior atividade antibacteriana frente E. coli e Enterobacter sakazakii (6.826 e 8.106 UA mL-1 respectivamente), moderada atividade frente a Salmonella enterica Enteritidis (1.600 UA mL-1) e não apresentou atividade frente a Listeria monocytogenes.Origanum majorana também foi testado neste estudo e apresentou maior atividade antimicrobiana frente E. coli (5.973 UA mL-1), atividade moderada para Salmonella enterica Enteritidis e Enterobacter sakazakii (1.706 e 2.346 UA mL-1 , respectivamente) e não apresentou atividade para Listeria monocytogenes. ABSTRACT The objective of this work was to identify and quantify the constituents, and to evaluate the antimicrobial activity of the essential oils from Mentha piperita, Cymbopogon citratus, Ocimum basilicum and Origanum majorana, against enteropathogenic Escherichia coli, Salmonella enterica Enteritidis, Listeria monocytogenes and Enterobacter sakazakii. The essential oils were obtained from dried leaves by using the hydrodistillation technique and the modified Clevenger apparatus, and their bacterial activity was determined by using the agar diffusion technique. The essential oils inhibited bacterial growth, but their effectiveness was varied. Among the essential oils tested, that from M. piperita showed a greater antimicrobial activity against E. coli (8.106 UA mL-1), moderate activity for S. enterica Enteritidis and E. sakazakii (1.706 e 3.200 UA mL-1 respectively) and low activity for L. monocytogenes (106,67 UA mL-1). However, the essential oil from C. citratus presented a greater antimicrobial activity against E. coli (9.386 UA mL-1) and a moderate activity against E. sakazakii, S. enterica Enteritidis and L. monocytogenes (2.773 UA mL-1 for both). The essential oil from O. basilicum showed a greater antimicrobial activity against E. coli and E. sakazakii (6.826 e 8.106 UA mL-1 respectively),moderate activity against S. enterica Enteritidis (1.600 UA mL-1), and was inactive against L, monocytogenes. Origanum majorana, which was also tested in our work, showed a greater antibacterial activity against E. coli, (5.973 UA mL-1) moderate activity against S. enterica Enteritidis and E. sakazakii (1.706 e 2.346 UA mL-1 , respectively), and was inactive against L. monocytogenes.

Myocardial damage in infancy is a risk factor for eventual cardiac disease. Given that myocardial stress is greatest during the perinatal period and that the neonatal period is when most pediatric heart failure occurs, the aim of this study was to determine whether even otherwise healthy neonates might have subclinical myocardial damage and, if so, what characteristics might identify them. Umbilical cord and neonatal serum samples from 32 normal neonates were assayed for biomarkers of myocardial injury. No neonate had clinical evidence of cardiac or other abnormalities. Serum cardiac troponin T was elevated in 19 of 25 cords (76%) and in 16 of 17 neonates (94%); levels indicating myocardial infarction (or =0.2 ng/ml) were found in 2 patients (1 umbilical cord and 1 neonatal sample). Creatine kinase-MB was elevated in 6 of 16 cords (38%) and in 8 of 15 neonates (53%). Cardiac troponin I was elevated in 11% and 17% of samples, myoglobin in 4% and 17%, and high-sensitivity C-reactive protein in 9% and 40%. Measures of myocardial injury were associated with longer hospitalization (r = 0.50, p = 0.04), non-Caucasian race (p = 0.012), lower birth weights (p = 0.014), positive maternal cervical cultures (r = 0.41, p = 0.046), and elevated high-sensitivity C-reactive protein (r = 0.66, p = 0.005). In conclusion, clinically occult myocardial injury appears to occur in some healthy newborns, although whether it is pathologic or not remains to be determined.

Cardiomyocyte injury in pediatric patients has a vast number of causes, which are often distinct from the causes of adult heart failure. However, the management of pediatric heart failure and heart transplantation has generally been inferred from adult studies. New therapies show great promise for the neurohormonal regulation of heart failure and the ability to control immunosuppression after heart transplantation. Large, randomized, multicenter, controlled clinical trials are needed to determine the efficacy of these therapies in this population. This article reviews the current recommendations and evidence-based medicine, where available, for the medical management of myopathic dysfunction and transplantation in pediatric patients.

Coronary artery disease (CAD) continues to be the leading cause of mortality and morbidity in developed countries. Assessment of pre-test probability (PTP) based on patient's characteristics, gender and symptoms, help to identify more accurate patient's clinical likelihood of coronary artery disease. Consequently, non-invasive imaging tests are performed more appropriately to rule in or rule out CAD rather than invasive coronary angiography (ICA). Coronary computed tomography angiography (CCTA) is the first-line non-invasive imaging technique in patients with suspected CAD and could be used to plan and guide coronary intervention. Invasive coronary angiography remains the gold-standard method for the identification and characterization of coronary artery stenosis. However, it is recommended in patients where the imaging tests are non-conclusive, and the clinical likelihood is very high, remembering that in clinical practice, approximately 30 to 70% of patients with symptoms and/or signs of ischemia, referred to coronary angiography, have non obstructive coronary artery disease (INOCA). In this contest, physiology and imaging-guided revascularization represent the cornerstone of contemporary management of chronic coronary syndromes (CCS) patients allowing us to focus specifically on ischemia-inducing stenoses. Finally, we also discuss contemporary medical therapeutic approach for secondary prevention. The aim of this review is to provide an updated diagnostic and therapeutic approach for the management of patients with stable coronary artery disease.

Harnessing the mechanisms underlying the exacerbated vascular remodelling in Diabetes Mellitus (DM) is pivotal to prevent the high toll of vascular diseases in DM patients. microRNAs (miRNA) regulate vascular smooth muscle cell (VSMC) phenotypic switch. However, miRNA modulation of the detrimental diabetic VSMC phenotype is underexplored. Streptozotocin-induced Type 1 Diabetes (T1DM) Wistar rats and T2DM Zucker rats underwent right carotid artery experimental angioplasty and global miRNA/mRNA expression profiling was obtained by RNA sequencing (RNA-Seq). 2 days after injury a set of 6 miRs were found to be uniquely down-regulated or up-regulated both in VSMCs in T1DM and T2DM. Among these, miR-29c and miR-204 were the most significantly mis-regulated in atherosclerotic plaques from DM patients. miR-29c overexpression and miR-204 inhibition per se attenuated VSMC phenotypic switch in DM. Concomitant miR-29c overexpression and miR-204 inhibition fostered an additive reduction in VSMC proliferation. Epithelial membrane protein 2 (Emp2) and Caveolin-1 (Cav1) mRNAs were identified as direct targets of miR-29c and miR-204, respectively. Importantly, contemporary miR-29c overexpression and miR-204 inhibition in the injured artery robustly reduced arterial stenosis in DM rats. Thus, contemporaneous miR-29c activation and miR-204 inhibition in DM arterial tissues is necessary and sufficient to prevent the exaggerated VSMC growth upon injury. Harnessing the mechanisms underlying the exacerbated vascular remodeling in diabetes mellitus (DM) is pivotal to prevent the high toll of vascular diseases in patients with DM. miRNA regulates vascular smooth muscle cell (VSMC) phenotypic switch. However, miRNA modulation of the detrimental diabetic VSMC phenotype is underex-plored. Streptozotocin-induced type 1 DM (T1DM) Wistar rats and type 2 DM (T2DM) Zucker rats underwent right carotid artery experimental angioplasty, and global miRNA/mRNA expression profiling was obtained by RNA sequencing (RNA-Seq). Two days after injury, a set of six miRNAs were found to be uniquely downregulated or upregulated in VSMCs both in T1DM and T2DM. Among these miRNAs, miR-29c and miR-204 were the most significantly misregulated in atherosclerotic plaques from patients with DM. miR-29c overexpression and miR-204 inhibition per se attenuated VSMC phenotypic switch in DM. Concomitant miR-29c overexpression and miR-204 inhibition fostered an additive reduction in VSMC proliferation. Epithelial membrane protein 2 (Emp2) and Caveolin-1 (Cav1) mRNAs were identified as direct targets of miR-29c and miR-204, respectively. Importantly, contemporary miR-29c overexpression and miR-204 inhibition in the injured artery robustly reduced arterial stenosis in DM rats. Thus, contemporaneous miR-29c activation and miR-204 inhibition in DM arterial tissues is necessary and sufficient to prevent the exaggerated VSMC growth upon injury.