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En el presente trabajo, pretendemos a la vez relatar y analizar la experiencia de acompañamiento de las trayectorias académicas de estudiantes que cursaron oportunamente la materia Didáctica y que aún, por diversos motivos, adeudan la acreditación del examen final. La iniciativa consiste en diseñar e implementar una serie de estrategias tendientes a acompañar al grupo de estudiantes que se encuentra en esta situación para que puedan finalmente acreditar la asignatura y proseguir su recorrido académico. Como estrategia, confeccionamos la nómina de las personas que cursaron la materia entre los años 2015- 2020, para identificar si aprobaron la cursada y corroborar si ya promovieron el final de la materia. En dicha nómina, además contamos con información de contacto de estudiantes para entablar una comunicación y a partir de allí, generar lo que llamamos “Mateadas Prefinales” que son espacios de acompañamiento y orientación en donde los y las estudiantes puedan plantear las necesidades, inquietudes y dificultades que se les presentan a la hora de prepararse para rendir el examen final de Didáctica. Esperamos que este artículo posibilite profundizar nuestra reflexión permanente como cátedra sobre las prácticas de enseñanza así como contribuir al mejoramiento de estrategias de acompañamiento de las trayectorias estudiantiles y de accesibilidad al derecho a la educación superior., In the present work, we intend to report and analyze the experience of monitoring the academic trajectories of students who took the Didactics subject in a timely manner and who still, for various reasons, owe the accreditation of the final exam. The initiative consists of designing and implementing a series of strategies aimed at accompanying the group of students who find themselves in this situation so that they can finally accredit the subject and continue their academic way. As a strategy, we first prepare the payroll of the people who took the course between 2015 and 2020, to identify if they passed the course and corroborate if they have already promoted the end of the course. In this list, we also have contact information for students to initiate communication and from there, generate what we call “Mateadas Prefinales” which are support and orientation spaces where students can raise their needs, concerns and difficulties that arise when preparing to take the final exam in Didactics We hope that this article will make it possible to deepen our permanent reflection as a chair on teaching practices as well as to contribute to the improvement of strategies for accompanying student trajectories and accessibility to the right to higher education., Especialización en Docencia Universitaria

Assays of cytokines in the plasma at the onset of graft-vs. -host disease (GVHD) can predict disease severity and treatment-related mortality (TRM); however, the optimal time during which cytokines should be tested and the specific panel of cytokines with the highest predictive ability remain unknown. We chose a predefined time point, 18 days after hematopoietic stem cell transplantation (HSCT), to measure the levels of six cytokines in the plasma: soluble interleukin-2 receptor alpha (sIL2-Rα), T-cell immunoglobulin domain and mucin domain-3 (TIM-3), suppression of tumorigenicity-2 (ST-2), intercellular adhesion molecule (ICAM-1), interferon-gamma (IFN-γ), and interleukin-6 (IL-6). The study included 95 patients, who underwent allogeneic hematopoietic transplantation at our institution. Plasma levels of sIL2-Rα and TIM-3, measured as continuous data, had predictive value for overall survival (sIL2-Rα, p = 0.002; TIM-3, p = 0.0007), while TRM could be predicted by sIL2-Rα (p = 0.0005), IFN-gamma (p = 0.01), and IL-6 (p = 0.0001). No cytokine was associated with the risk of relapse. Patients were categorized into groups, according to cytokine thresholds determined by receiver operating characteristic curve analysis (sIL2-Rα ≤ or > 8,100 pg/ml; TIM-3 ≤ or > 950 pg/ml) and multivariate analysis was conducted. High levels of both TIM-3 and sIL2-Rα were significant predictors of poor survival [TIM-3 > 950 pg/ml: hazard ratio (HR) = 6.214 (95% CI 1.939–19.910), p = 0.002 and sIL2-Rα > 8.100 pg/ml: HR = 2.644 (95% CI 1.308–5.347), p = 0.006]. Using these cutoff thresholds, we constructed a composite scoring system that could distinguish three different groups of patients with varying rates of TRM: high risk, 41.7%; intermediate risk, 10.8%; and low risk, 7.1% (Gray's test: p = 0.001). If confirmed in a validation cohort, this composite scoring system could be used to guide the modulation of post-transplant immune suppressive therapy.

Mounting evidence points to immune-mediated synaptopathy and impaired plasticity as early pathogenic events underlying cognitive decline (CD) in Multiple sclerosis (MS) and in the experimental autoimmune encephalomyelitis (EAE) mouse model of the disease. However, knowledge of the neurobiology of synaptic dysfunction is still incomplete. Splicing regulation represents a flexible and powerful mechanism involved in dynamic remodeling of the synapse, which allows the expression of synaptic protein variants that dynamically control the specificity of contacts between neurons. The pre-synaptic adhesion molecules neurexins (NRXNs) 1-3 play a relevant role in cognition and are alternatively spliced to yield variants that differentially cluster specific ligands in the postsynaptic compartment and modulate functional properties of the synaptic contact. Notably, mutations in these genes or disruption of their splicing program are associated with neuropsychiatric disorders. Herein, we have investigated how inflammatory changes imposed by EAE impact on alternative splicing of the Nrxn 1-3 mouse genes in the acute phase of disease. Due to its relevance in cognition, we focused on the prefrontal cortex (PFC) of SJL/J mice, in which EAE-induced inflammatory lesions extend to the rostral forebrain. We found that inclusion of the Nrxn 1-3 AS4 exon is significantly increased in the PFC of EAE mice and that splicing changes are correlated with local Il1β-expression levels. This correlation is sustained by the concomitant downregulation of SLM2, the main splicing factor involved in skipping of the AS4 exon, in EAE mice displaying high levels of Il1β- expression. We also observed that Il1β-expression levels correlate with changes in parvalbumin (PV)-positive interneuron connectivity. Moreover, exposure to environmental enrichment (EE), a condition known to stimulate neuronal connectivity and to improve cognitive functions in mice and humans, modified PFC phenotypes of EAE mice with respect to Il1β-, Slm2-expression, Nrxn AS4 splicing and PV-expression, by limiting changes associated with high levels of inflammation. Our results reveal that local inflammation results in early splicing modulation of key synaptic proteins and in remodeling of GABAergic circuitry in the PFC of SJL/J mice. We also suggest EE as a tool to counteract these inflammation-associated events, thus highlighting potential therapeutic targets for limiting the progressive CD occurring in MS.

AimsThe presence of cold agglutinin in blood samples can cause a spontaneous agglutination of red blood cells (RBCs) when low temperature occurs. This phenomenon causes a spurious lowering of RBC count on the automated haematological analysers that are detected by incongruous values (≥370 g/L) of the mean cellular haemoglobi concentration (MCHC). A preheating at 37°C can remove the RBC agglutination generally resulting in a reliable count. It has been reported that the same result can be reached by using the optical reticulocyte (RET) channel of Sysmex analysers where the RBC count is not influenced by the presence of cold agglutinin. This study aims to evaluate these data in a larger population, with regard to environmental conditions on Sysmex analysers. We have also evaluated the influence of different thermal pretreatments on the RBC count.MethodsThis study was performed on 96 remnants of peripheral blood samples (48 with MCHC in normal range and 48 with MCHC>370 g/L) which have been analysed in different preanalytical conditions on the Sysmex analysers.ResultsA preheating of samples at 41°C for 1 min leads to a reversibility of the cold agglutination comparable to the one observed in the RET channel and yields better results compared with 37°C for 2 hours.ConclusionsNone of described procedures assure the complete cold agglutination reversibility in every case. Consequently, since the haematological analysers not yet provide reliable parameters to confirm the complete resolution of agglutination, further verification of RBC count accuracy needs to be performed.

S100B is a Ca2+ -binding protein mainly concentrated in astrocytes. Its levels in biological fluids (cerebrospinal fluid, peripheral and cord blood, urine, saliva, amniotic fluid) are recognized as a reliable biomarker of active neural distress. Although the wide spectrum of diseases in which the protein is involved (acute brain injury, neurodegenerative diseases, congenital/perinatal disorders, psychiatric disorders) reduces its specificity, its levels remain an important aid in monitoring the trend of the disorder. Mounting evidence now points to S100B as a Damage-Associated Molecular Pattern molecule which, when released at high concentration, through its Receptor for Advanced Glycation Endproducts, triggers tissue reaction to damage in a series of different neural disorders. This review addresses this novel scenario, presenting data indicating that S100B levels and/or distribution in the nervous tissue of patients and/or experimental models of different neural disorders, for which the protein is used as a biomarker, are directly related to the progress of the disease: acute brain injury (ischemic/hemorrhagic stroke, traumatic injury), neurodegenerative diseases (Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, multiple sclerosis), congenital/perinatal disorders (Down syndrome, spinocerebellar ataxia-1), psychiatric disorders (schizophrenia, mood disorders), inflammatory bowel disease. In many cases, over-expression/administration of the protein induces worsening of the disease, whereas its deletion/inactivation produces amelioration. This review points out that the pivotal role of the protein resulting from these data, opens the perspective that S100B may be regarded as a therapeutic target for these different diseases, which appear to share some common features reasonably attributable to neuroinflammation, regardless their origin.

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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by a non-cell autonomous motor neuron loss. While it is generally believed that the disease onset takes place inside motor neurons, different cell types mediating neuroinflammatory processes are considered deeply involved in the progression of the disease. On these grounds, many treatments have been tested on ALS animals with the aim of inhibiting or reducing the pro-inflammatory action of microglia and astrocytes and counteract the progression of the disease. Unfortunately, these anti-inflammatory therapies have been only modestly successful. The non-univocal role played by microglia during stress and injuries might explain this failure. Indeed, it is now well recognized that, during ALS, microglia displays different phenotypes, from surveillant in early stages, to activated states, M1 and M2, characterized by the expression of respectively harmful and protective genes in later phases of the disease. Consistently, the inhibition of microglial function seems to be a valid strategy only if the different stages of microglia polarization are taken into account, interfering with the reactivity of microglia specifically targeting only the harmful pathways and/or potentiating the trophic ones. In this review article, we will analyze the features and timing of microglia activation in the light of M1/M2 phenotypes in the main mice models of ALS. Moreover, we will also revise the results obtained by different anti-inflammatory therapies aimed to unbalance the M1/M2 ratio, shifting it towards a protective outcome.

By taking advantage of a "floxed" conditional CREB mutant mouse (CREB1loxP/loxP), in which postnatal deletion of the Creb gene in the forebrain is driven by the calcium/calmodulin-dependent protein kinase II-α gene (Camk2a) promoter (BCKO mice), we here show that selective disruption of CREB function in adult forebrain neurons results, in adult mice, in morphological alterations at the hippocampal level, including hippocampal shrinkage, reduced somal volume of neurons, microgliosis and mild reactive astrocytosis, mainly involving the CA1 subfield. The huge increase of microglial cells showing a mild activated profile, and the higher percentage of double-stained GFAP/S100B astrocytes, together with the increased expression of S100b mRNA at hippocampal level, suggest the establishment of a sub-inflammatory environment in the hippocampus of BCKO mice compared with age-matched controls. Collectively, the present data link neuron-specific, adult deletion of CREB to hippocampal structural alterations and to the early appearance of neuropathological features closely resembling those occurring in the aged brain. This information may be valuable for the understanding of the role of CREB in neuroinflammatory pathways.

Background/Aims: An important public health issue is monitoring folate inadequacy in women of childbearing potential. The aim of the present study was to investigate associations between folate intake, red blood cell (RBC) folate, total homocysteine (tHcy) and the MTHFR 677T allele. Methods: A total of 204 women were enrolled in a cross-sectional study. Folate intake was assessed by a food frequency questionnaire, and RBC folate, tHcy and MTHFR C677T genotype were determined. Results: About half of the women had a decreased RBC folate level (Conclusions: Our study revealed significant folate deficiency in our Mediterranean population and higher than ideal Hcy concentrations, thus emphasizing that in these groups an improvement in the folate status is needed via a food-based approach or supplement. Consequently, public health policy strategies aiming at improved supplementation are required.

The selective vulnerability of specific neuronal subpopulations to trimethyltin (TMT), an organotin compound with neurotoxicant effects selectively involving the limbic system and especially marked in the hippocampus, makes it useful to obtain in vivo models of neurodegeneration associated with behavioural alterations, such as hyperactivity and aggression, cognitive impairment as well as temporal lobe epilepsy. TMT has been widely used to study neuronal and glial factors involved in selective neuronal death, as well as the molecular mechanisms leading to hippocampal neurodegeneration (including neuroinflammation, excitotoxicity, intracellular calcium overload, mitochondrial dysfunction and oxidative stress). It also offers a valuable instrument to study the cell-cell interactions and signalling pathways that modulate injury-induced neurogenesis, including the involvement of newly generated neurons in the possible repair processes. Since TMT appears to be a useful tool to damage the brain and study the various responses to damage, this review summarises current data from in vivo and in vitro studies on neuroprotective strategies to counteract TMT-induced neuronal death, that may be useful to elucidate the role of putative candidates for translational medical research on neurodegenerative diseases.

Given the well-documented involvement of estrogens in the modulation of hippocampal functions in both physiological and pathological conditions, the present study investigates the effects of 17-beta estradiol (E2) administration in the rat model of hippocampal neurodegeneration induced by trimethyltin (TMT) administration (8 mg/kg), characterized by loss of pyramidal neurons in CA1, CA3/hilus hippocampal subfields, associated with astroglial and microglial activation, seizures and cognitive impairment. After TMT/saline treatment, ovariectomized animals received two doses of E2 (0.2 mg/kg intra-peritoneal) or vehicle, and were sacrificed 48 h or 7 days after TMT-treatment. Our results indicate that in TMT-treated animals E2 administration induces the early (48 h) upregulation of genes involved in neuroprotection and synaptogenesis, namely Bcl2, trkB, cadherin 2 and cyclin-dependent-kinase-5. Increased expression levels of glutamic acid decarboxylase (gad) 67, neuropeptide Y (Npy), parvalbumin, Pgc-1α and Sirtuin 1 genes, the latter involved in parvalbumin (PV) synthesis, were also evident. Unbiased stereology performed on rats sacrificed 7 days after TMT treatment showed that although E2 does not significantly influence the extent of TMT-induced neuronal death, significantly enhances the TMT-induced modulation of GABAergic interneuron population size in selected hippocampal subfields. In particular, E2 administration causes, in TMT-treated rats, a significant increase in the number of GAD67-expressing interneurons in CA1 stratum oriens, CA3 pyramidal layer, hilus and dentate gyrus, accompanied by a parallel increase in NPY-expressing cells, essentially in the same regions, and of PV-positive cells in CA1 pyramidal layer. The present results add information concerning the role of in vivo E2 administration on mechanisms involved in cellular plasticity in the adult brain.

This article aims to analyze Faris Antonio Salomao Michaele's intellectual trajectory (1911-1977) and discuss his conception of education. Faris Michaele was...

Several dietary agents, such as micronutrient and non-nutrient components, the so-called bioactive food components, have been shown to display anticancer properties and influence genetic processes. The most common epigenetic change is DNA methylation. Hypomethylation of long interspersed elements (LINE-1) has been associated with an increased risk of several cancers, although conflicting findings have also been observed. The aim of the present study was to test the hypothesis that a low adherence to the Mediterranean diet (MD) and folate deficiency may cause LINE-1 hypomethylation in blood leukocytes of healthy women, and thus genomic instability. One hundred and seventy-seven non-pregnant women were enrolled. Mediterranean diet score (MDS) and folate intake were calculated using a food frequency questionnaire. LINE-1 methylation level was measured by pyrosequencing analysis in three CpG sites of LINE-1 promoter. According to MDS, only 9.6 % of subjects achieved a high adherence to MD. Taking into account the use of supplements, there was a high prevalence of folate deficiency (73.4 %). Women whose consumption of fruit was below the median value (i.e.

To verify the hypothesis of an early impairment of erythropoietin (Epo) production and to assess the adequacy of its circulating levels in diabetic nephropathy, we investigated Epo values in 18 microalbuminuric type 2 diabetic patients with normal renal function (7 anaemic and 11 nonanaemic), 24 subjects with uncomplicated iron-deficiency anaemia, and 15 healthy controls comparable for sex and age. Mean±S.D. plasma Epo level was 56.4±12.7 mU/mL in iron-deficient patients and 9.3±2.6 mU/mL in controls. In diabetic groups, mean±S.D. Epo level was 11.38±3.65 mU/mL in nonanaemic and 49.12±6.44 mU/mL in anaemic subjects. No significant difference ( P >.05) in Epo values was found between controls and nonanaemic diabetic patients. Anaemic diabetics and iron-deficient subjects had significantly higher values than the nonanaemic groups ( P >.001). An inverse significant relation between Epo levels and Hb concentration resulted in both anaemic diabetics ( r =−.44, P >.05) and iron-deficient patients ( r =−.61, P =.001). Analysis of covariance ( P >.05) and comparison of the two regression lines ( t =0.4, df =29, P >.05) did not show any significant difference between diabetic patients with anaemia and iron-deficient patients. These results suggest that normochromic anaemia observed in microalbuminuric diabetic patients with normal renal function is not due to Epo deficiency, and circulating levels of this hormone are suitably increased with regard to Hb concentration.

Background The overuse and misuse of antibiotics, has contributed to the selection, emergence and dissemination of resistant pathogens. The objective of the study is to provide an overview of changes in antibiotic consumption and resistance data in two Intensive Care Units (ICU1 and ICU2) during a six-years period, from 2008 to 2013. Methods The study used a laboratory-based surveillance approach. Antimicrobial resistance rates (RR) were calculated as the number of resistant isolates divided by the total …

The mitochondrial DNA (mtDNA) 4977-bp deletion is a biomarker of mitochondrial genomic instability. It is frequently detected in a number of sporadic diseases, and it accumulates in many tissues during aging. Folic acid plays an important role in the maintenance of genomic stability in mammals. The aim of the present cross-sectional study was to characterise the levels of the mtDNA deletion in the lymphocytes of healthy young women, taking into account folate intake, red blood cell (RBC) folate levels and the distribution of the methylenetetrahydrofolate reductase (MTHFR) gene C677T polymorphism. Folate intake was estimated by a food frequency questionnaire. Determination of the MTHFR C677T polymorphism and of the mtDNA deletion was performed by real-time polymerase chain reaction analysis. A total of 476 women were enrolled. Low levels of deletion were found (mean ?Ct = 1.24). After multivariate analysis, results did not show any significant relationship between age, smoking habits, pregnancy status, nutritional status, inadequate folate intake, folate deficiency, use of folic acid supplements, MTHFR C677T polymorphism and mtDNA 4977-bp deletions. The lack of association between inadequate folate intake, folate deficiency and mitochondrial genomic instability was confirmed also considering reference values of folate based on DNA damage prevention. Our results indicate that mtDNA 4977-bp deletions are maintained at low levels in lymphocytes of young healthy women despite the wide range of variation of folate intakes and folate status. Future studies, carefully designed to address limits and methodological issues related to variation of this biomarker as an effect of different dietary patterns and of folate status, could provide further insight on the specific mechanisms that are acting in lymphocytes of healthy subjects under observed folate intake. © 2014 © The Author 2014. Published by Oxford University Press on behalf of the UK Environmental Mutagen Society. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

The present study was conducted in order to (i) characterize the adherence to the Mediterranean diet (MD) pattern and fatty acids (FAs) intakes and (ii) explore interactions betweenTNFA−308 G>A polymorphism and adherence to MD and FAs intakes, respectively, on overweight/obesity risk. From 2010 to 2013, 380 healthy women were enrolled, and MD score (MDS) and FAs intakes were evaluated by a Food Frequencies Questionnaire in relation to nutritional status.TNFA−308 G/A polymorphism was characterized using PCR-RFLP. A total of 32.6% of women were overweight or obese. Lower mean MDS values were more observed in the younger age group than in the older age group (3.60 versus 4.45). The risk of being overweight/obese was 3.5-fold increased due to poor adherence to MD and was about twofold increased in less educated women. Furthermore, younger age was associated with poor adherence to MD. No evidence for an independent effect of the polymorphism on overweight/obesity risk was found. There was no evidence of biological interaction from the gene-diet interaction analyses. Young women, less educated and with poor adherence to MD, are a target group for the nutritional interventions that aimed to control the obesity risk, thus improving the adherence to MD and particularly the intake of unsaturated FAs.

El siguiente trabajo pretende realizar un análisis cualitativo de algunas de las propuestas virtuales en internet para la enseñanza de la historia reciente en las escuelas secundarias de la provincia de Buenos Aires. La implementación del Programa «Conectar Igualdad» en las escuelas argentinas no sólo interpeló a los docentes a modificar sus prácticas de enseñanza, sino que llevó a que los estudiantes revisen sus estrategias de aprendizaje generando un paquete de actividades en la Web y articulando múltiples y variados recursos para la enseñanza que están al alcance de todos. Sin embargo, no todos los materiales que se encuentran disponibles son revisados y pertinentes para utilizarlos en las escuelas, sino que deben ser analizados y adecuados a las características de los contextos de implementación., The present paper tries to discuss some questions about the uses and possibilities of virtual materials in teaching in recent history. For that, we analysis three didactic sequences thinking for the secondary school. he «Conectar Igualdad» program in the Argentinean school, not only questioning the teachers and push them into new teaching practices but it also modiies some learning strategies. his program which it was created by the National Government give every student and teacher a netbook and moreover, opened a portal called Educ.ar to ofer a package of virtual materials.Even though, not all the virtual materials for the teaching in recent history are good for learning in the secondary schools and they must be revised an analyzed in order to their use in that context., Facultad de Humanidades y Ciencias de la Educación

The effects of intracerebroventricular administration of neuropeptide Y (NPY), which is believed to play an important role in neuroprotection against excitotoxicity and in the modulation of adult neurogenesis, were evaluated in an animal model of hippocampal neurodegeneration and temporal lobe epilepsy represented by trimethyltin (TMT) intoxication. A single TMT injection (8 mg/kg) causes, in the rat brain, massive neuronal death, selectively involving pyramidal neurons, accompanied by glial activation and enhanced hippocampal neurogenesis. Our data indicate that intracerebroventricular administration of exogenous NPY (at the dose of 2 μg/2 μL, 4 days after TMT-administration), in adult rats, exerts a protective role in regard to TMT-induced hippocampal damage and a proliferative effect on the hippocampal neurogenic niche through the up-regulation of Bcl-2, Bcl2l1, Bdnf, Sox-2, NeuroD1, Noggin and Doublecortin genes, contributing to delineate more clearly the role of NPY in in vivo neurodegenerative processes.

Folate has been recognized to ensure reproductive health and there is a growing body of epidemiological evidence suggesting that the methylenetetrahydrofolate reductase (MTHFR) 677T allele and reduced dietary folate may increase the risk of cervical cancer. The main focus of our survey was to investigate the distribution of the MTHFR C677T polymorphism in relation to women's year of birth and to assess their folate intake and folic acid supplementation.During a 6-months period, 307 healthy women of childbearing age in Catania, Italy, were enrolled in the cross-sectional study. Folate intake was estimated by a semiquantitative food frequency questionnaire and DNA extracted from blood samples for MTHFR C677T genotyping.A TT genotype frequency of 20.5% with an increase in the prevalence of the TT genotype in the cohort of women born since 1959 was shown. The prevalence of inadequate folate intake was 51.5%, significantly higher in non-pregnant women (83.4%) than in pregnant ones (12.3%) with a decrease during the three trimesters of pregnancy (from 25.7 to 5.0%; P=0.013). The use of folic acid supplements improved during the three trimester of pregnancy (from 71.4 to 95.0%; P=0.001).Healthy young women may have higher folate needs due to increasing prevalence of the T allele and reduced folate intake compared with older groups. However, clinicians should be cautious when recommending supplements to women in late pregnancy due to the possible implications in the pregnancy outcome.

AIM: In the inflammatory state, intercellular adhesion molecule-1 (ICAM-1) and vascular cellular adhesion molecule-1 (VCAM-1) play a key role in promoting migration of immunological cells from the circulation to target site. Aim of our study was to investigate soluble forms of these molecules in patients with virus-related chronic liver diseases, to assess their behavior in different pathologies and correlation with severity of liver damage. METHODS: Circulating ICAM-1 and VCAM-1 were assayed by EIA commercial kits (R&D System Co., Abington, UK) in 23 patients with chronic active hepatitis (CH), 50 subjects affected by liver cirrhosis (LC) and 15 healthy controls comparable for sex and age. In patients, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were also detected by autoanalyzer. RESULTS: LC patients had significantly higher ICAM-1 values than CH patients (38.567.4 ng/mL vs 20.896.42 ng/mL; P

Background The overuse of antimicrobials is one of the main factors responsible for the development and spread of antimicrobial resistance, together with other causes, such as intra- and inter-hospital spread of resistant microorganisms and infection control policies and practices. The objective of the present study is to report the trends of Klebsiella pneumoniae and Acinetobacter baumannii antimicrobial resistance indicators in an Italian intensive care unit (ICU) during a six-year period, from 2008 to 2013. Methods Susceptibility data and annual antibiotic consumptions in the ICU were retrospectively obtained from the clinical laboratory and the pharmacy. Trends over time of resistance rates (RRs) and of incidence densities of resistant isolates were determined by linear regression. Results Isolation density of A. baumannii increased significantly from 2008 (20.4 per 1,000 patient-days) to 2013 (58.1 per 1,000 patient-days) and of K. pneumoniae from 2010 (22.3 per 1,000 patient-days) to 2013 (55.9 per 1,000 patient-days). RRs of third-generation cephalosporins (3GCs)-resistant K. pneumoniae (from 2010: 41.9 %, to 2012: 87.0 %), of carbapenem-resistant K. pneumoniae (from 2008: 0 %, to 2013: 59.2 %), and of carbapenem-resistant A. baumannii (from 2008: 87.5 %, to 2013: 96.6 %) showed significant increasing trends. Carbapenems was the main antibiotic class consumed (24.9 % of the total antimicrobial usage density), followed by 3GCs (21.0 %), fluoroquinolones (20.6 %), aminoglycosides (17.3 %), penicillins (15.1 %) and glycopeptides (1.1 %). Carbapenems consumption decreased from 2008 to 2012 and then increased in 2013. Glycopeptides consumption decreased from 2008 to 2011 and then increased in 2013. Aminoglycosides consumption decreased from 2008 to 2010 and increased from 2012 to 2013. Finally, 3GC, penicillins and fluoroquinolones consumptions decreased from 2012 to 2013. Conclusions RRs of carbapenem-resistant A. baumannii and of carbapenem- and 3GC-resistant K. pneumoniae were higher than those for Europe. Our findings highlight the necessity to implement an integrated system for monitoring not only consumption of antibiotics and resistance profiles but also the clonality of alert microorganisms in the ICU for effective infection control.