University quality measurement model based on balanced scorecard

A Higher Education Institution (HEI) has the responsibility to track the processes through indicators that guarantee the measurement of the results in almost real time. This article presents the design of a management and quality model of the processes in a university, through the integration of a Balance Scorecard (BSC) and the implementation of an information system. For which it was required: a review of existing tracing and monitoring systems in the academic sector, definition of the requirements of the proposed technological, a diagnosis of the current measurement system of the HEI analyzed, identify measurement indicators and develop a technological tool. The designed model presents a precise and clear methodological guide that can be replicated in any HEI to monitor its processes

Cardiac ion channels associated with unexplained stillbirth - an immunohistochemical study

OBJECTIVES: Despite the use of post-mortem investigations, approximately 20% of stillbirths remain unexplained. Cardiac ion channelopathies have been identified as a cause of death in Sudden Infant Death Syndrome (SIDS) and could be associated with unexplained stillbirths. This study aimed to understand if the expression or localisation of cardiac ion channels associated with channelopathies were altered in cases of unexplained stillbirths.METHODS: A case control study was conducted using formalin-fixed cardiac tissue from 20 cases of unexplained stillbirth and a control group of 20 cases of stillbirths from intrapartum hypoxia. 4 µm tissue sections were stained using haematoxylin and eosin, Masson's trichrome (MT) and Elastic van Gieson (EVG). Immunohistochemistry (IHC) was performed using antibodies against CACNA1G, KCNJ2, KCNQ1, KCNH2 and KCNE1. The cardiac conduction system in samples stained with MT and EVG could not be identified. Therefore, the levels of immunoperoxidase staining were quantified using QuPath software.RESULTS: The nuclear-cytoplasmic ratio of sections stained with haematoxylin and eosin was higher for the hypoxia group (hypoxia median 0.13 vs. 0.04 unexplained, p &lt; 0.001). CACNA1G (unexplained median 0.26 vs. hypoxia 0.30, p=0.009) and KCNJ2 (unexplained median 0.35 vs. hypoxia 0.41, p=0.001) had lower staining intensity in the unexplained stillbirth group. There were no statistically significant differences in the staining intensity of KCNQ1, KCNH2 and KCNE1.CONCLUSIONS: Two ion channels associated with channelopathies demonstrated lower levels of expression in cases of unexplained stillbirth. Further genetic studies using human tissue should be performed to understand the association between channelopathies and otherwise unexplained stillbirths.</p

Loss of hippocampal neurons after kainate treatment correlates with behavioral deficits.

Treating rats with kainic acid induces status epilepticus (SE) and leads to the development of behavioral deficits and spontaneous recurrent seizures later in life. However, in a subset of rats, kainic acid treatment does not induce overt behaviorally obvious acute SE. The goal of this study was to compare the neuroanatomical and behavioral changes induced by kainate in rats that developed convulsive SE to those who did not. Adult male Wistar rats were treated with kainic acid and tested behaviorally 5 months later. Rats that had experienced convulsive SE showed impaired performance on the spatial water maze and passive avoidance tasks, and on the context and tone retention tests following fear conditioning. In addition, they exhibited less anxiety-like behaviors than controls on the open-field and elevated plus-maze tests. Histologically, convulsive SE was associated with marked neuron loss in the hippocampal CA3 and CA1 fields, and in the dentate hilus. Rats that had not experienced convulsive SE after kainate treatment showed less severe, but significant impairments on the spatial water maze and passive avoidance tasks. These rats had fewer neurons than control rats in the dentate hilus, but not in the hippocampal CA3 and CA1 fields. Correlational analyses revealed significant relationships between spatial memory indices of rats and neuronal numbers in the dentate hilus and CA3 pyramidal field. These results show that a part of the animals that do not display intense behavioral seizures (convulsive SE) immediately after an epileptogenic treatment, later in life, they may still have noticeable structural and functional changes in the brain

R2CHA2DS2-VA predictsthe cardiovascular risk after carotid endarterectomy

Background: R2CHA2DS2-VA score has been used to predict short and long-term outcomes in many cardiovascular diseases. This study aims to validate the R2CHA2DS2-VA score as a long-term major adverse cardiovascular events (MACE) predictor after carotid endarterectomy (CEA). Secondary outcomes were also assessed regarding the incidence of all-cause mortality, acute myocardial infarction (AMI), major adverse limb events (MALE), and acute heart failure (AHF).Methods: From January 2012 to December 2021, patients (n 1/4 205) from a Portuguese tertiary care and referral center that underwent CEA with regional anesthesia (RA) for carotid stenosis (CS) were selected from a previously collected prospective database, and a posthoc analysis was performed. Demographics and comorbidities were registered. Clinical adverse events were assessed 30 days after the procedure and in the subsequent long-term surveillance period. Statistical analysis was performed by the Kaplan-Meier method and Cox proportional hazards regression.Results: Of the patients enrolled, 78.5% were males with a mean age of 70.44 & PLUSMN; 8.9 years. Higher scores of R2CHA2DS2-VA were associated with long-term MACE (adjusted hazard ratio (aHR) 1.390; 95% confidence interval (CI) 1.173-1.647); and mortality (aHR 1.295; 95% CI 1.08-1.545). Conclusions: This study demonstrated the potential of the R2CHA2DS2-VA score to predict long-term outcomes, such as AMI, AHF, MACE, and all-cause mortality, in a population of pa-tients submitted to carotid endarterectomy.info:eu-repo/semantics/publishedVersio

Loss of hippocampal neurons in kainate-treated rats.

<p>The y-axes represent the total numbers of neurons (mean±SD) in the dentate hilus and hippocampal CA3 and CA1 pyramidal fields in control rats and in kainate-treated rats with and without behavioral status epilepticus (BSE group and no-BSE group, respectively). The number of hilar neurons is reduced in both groups of kainate-treated rats when compared to control group. Note that the number of cells in the CA3 and CA1 pyramidal regions was strikingly reduced in rats from the BSE group, but not in those from the no-BSE group. Dentate hilus: *<i>p</i><0.05 for no-BSE group vs. control group and <i>p</i><0.01 for BSE group vs. control group; CA3 and CA1 fields: *<i>p</i><0.001 vs. control group and ^#<i>p</i><0.001 vs. no-BSE group.</p

Kainate-induced loss of neurons in the ventral dentate hilus.

<p>Photomicrographs of representative Nissl-stained coronal sections containing the ventral portion of the dentate gyrus taken from a control rat (<b>A</b>), from a rat in the behavioral status epilepticus (BSE) group (<b>B</b>) and from a kainate-treated rat that had not experienced behavioral status epilepticus (no-BSE; <b>C</b>). Note that the density of neurons in the dentate hilus is dramatically reduced in the rat that experienced behavioral SE (<b>B</b>). In striking contrast, most of the neurons of the ventral hilus are preserved in the rat from the no-BSE group (<b>C</b>). Scale bar shown in (<b>B</b>) = 250 µm.</p