Self-care behaviours and their relationship with Satisfaction and Compassion Fatigue levels among social workers.

Compassion fatigue is a syndrome resulting from an empathic listening to the client's distress. Social workers, by the relational nature of their task, can be at risk and may suffer from adverse health effects. This quantitative research (N = 270) aimed to assess the efficiency of social workers' self-care practices. The conclusion is that personal and professional self-care practices reduce compassion fatigue levels as well as increase satisfaction levels. Promoting self-care practices will bring benefits for the professional and, therefore, in the client and the institution.

[Renal replacement therapy in Intensive Care Units in Catalonia (Spain)]. / Utilización de las terapias de depuración extracorpórea en los Servicios de Medicina Intensiva de Cataluña (España).

OBJECTIVE: To assess the indications, settings and techniques used in renal replacement therapy (RRT) in Intensive Care Units (ICUs). STUDY DESIGN: A prospective, multicenter observational study was carried out. SETTING: Intensive Care Units. PATIENTS: All patients admitted to ICUs during the two-month study period in 2011 who required RRT. INTERVENTIONS: None. VARIABLES OF INTEREST: Patient demographic characteristics, baseline clinical data, RRT technique and materials used. RESULTS: Thirty-three patients were analyzed. RRT was started within the first 24hours after ICU admission in 17 of the 33 patients (52%). At the start of RRT, 18% of the patients (n=6) presented grade R on the RIFLE acute kidney injury (AKI) scale. The most common disorder associated with AKI was multiple organ dysfunction syndrome (64%; n=21). At the start of RRT, most patients (76%; n=25) presented hemodynamic instability, while the remaining 24% (n=8) were considered hemodynamically stable. The most common RRT technique in hemodynamically stable patients was continuous renal replacement therapy (CRRT) (63%; n=5). CRRT was the technique of choice in all 25 of the hemodynamically unstable patients (100%). Anticoagulation was used in 55% (n=18) of the patients. In most cases (61%, n=20), RRT was administered through the right femoral vein. In 84% (n=28) of the patients, the ultrafiltration effluent flow rate was ≤ 35ml/kg/h. CONCLUSIONS: The ICU physicians in this study followed current RRT guidelines. CRRT was preferred over intermittent renal replacement therapy, regardless of patient hemodynamic status.

Smad3 is required for the survival of proliferative intermediate progenitor cells in the dentate gyrus of adult mice.

BACKGROUND: New neurons are continuously being generated in the adult hippocampus, a phenomenon that is regulated by external stimuli, such as learning, memory, exercise, environment or stress. However, the molecular mechanisms underlying neuron production and how they are integrated into existing circuits under such physiological conditions remain unclear. Indeed, the intracellular modulators that transduce the extracellular signals are not yet fully understood. RESULTS: We show that Smad3, an intracellular molecule involved in the transforming growth factor (TGF)-ß signaling cascade, is strongly expressed by granule cells in the dentate gyrus (DG) of adult mice, although the loss of Smad3 in null mutant mice does not affect their survival. Smad3 is also expressed by adult progenitor cells in the subgranular zone (SGZ) and more specifically, it is first expressed by Type 2 cells (intermediate progenitor cells). Its expression persists through the distinct cell stages towards that of the mature neuron. Interestingly, proliferative intermediate progenitor cells die in Smad3 deficiency, which is associated with a large decrease in the production of newborn neurons in Smad3 deficient mice. Smad3 signaling appears to influence adult neurogenesis fulfilling distinct roles in the rostral and mid-caudal regions of the DG. In rostral areas, Smad3 deficiency increases proliferation and promotes the cell cycle exit of undifferentiated progenitor cells. By contrast, Smad3 deficiency impairs the survival of newborn neurons in the mid-caudal region of the DG at early proliferative stages, activating apoptosis of intermediate progenitor cells. Furthermore, long-term potentiation (LTP) after high frequency stimulation (HFS) to the medial perforant path (MPP) was abolished in the DG of Smad3-deficient mice. CONCLUSIONS: These data show that endogenous Smad3 signaling is central to neurogenesis and LTP induction in the adult DG, these being two forms of hippocampal brain plasticity related to learning and memory that decline with aging and as a result of neurological disorders.

Assay of acetylcholinesterase activity by potentiometric monitoring of acetylcholine.

An acetylcholine-selective electrode based on a plasticized polymeric membrane has been developed. The electrode exhibited good selectivity for acetylcholine (ACh) over choline and some common ions, low drift, and a fast response to ACh. The response was linear over an ACh concentration range of 1×10(-6) to 1×10(-3) M with a slope of 59.1±0.1 and a detection limit of 1.5×10(-7)±1.2×10(-8) M. The electrode was used to monitor enzymatic ACh hydrolysis catalyzed by acetylcholinesterase (AChE) at different substrate and enzyme concentrations. A kinetic data analysis permitted the determination of the Michaelis-Menten constant of the enzymatic hydrolysis and AChE activity in the range of 2×10(-5) to 3.8×10(-1)U ml(-1).

[From the laboratory to the clinic in acute ischaemic stroke. In vitro and in vivo experimental models]. / Del laboratorio a la clínica en el ictus isquémico agudo. Modelos experimentales in vitro e in vivo.

INTRODUCTION: Cerebrovascular disease is one of the leading causes of death, disability and dementia around the world. For the most common form of the disease, ischaemic stroke, there is only one drug available, tissue plasminogen activator, and few patients can benefit from this therapy because of the strict inclusion criteria established for its use. This circumstance makes it crucial to search for new forms of treatment to combat the sequelae of the disease, and this requires the development of new biomimetic models that allow for a better understanding of its evolution. DEVELOPMENT: In this review, we update the platforms and models most widely used in recent years to study the pathophysiology of ischaemic stroke. On the one hand, we review the two- and three-dimensional platforms on which in vitro assays are carried out and, on the other, we describe the most commonly used in vivo experimental models and techniques for assessing ischaemic damage. CONCLUSIONS: The ultimate aim of developing good experimental models is to find new forms of treatment and thus improve patients' prognosis and quality of life. It is therefore important to generate new in vitro devices and to further refine in vivo models to enable a good clinical translation.

TITLE: Del laboratorio a la clínica en el ictus isquémico agudo. Modelos experimentales in vitro e in vivo.Introducción. La enfermedad cerebrovascular es una de las principales causas de muerte, discapacidad y demencia en el mundo. La forma más frecuente de la enfermedad, el ictus isquémico, sólo tiene un fármaco disponible, el activador tisular del plasminógeno, y pocos pacientes pueden beneficiarse de esta terapia por los estrictos criterios de inclusión establecidos para su uso. Esta circunstancia hace crucial la búsqueda de nuevas formas de tratamiento para combatir las secuelas de la enfermedad, y para ello es necesario el desarrollo de nuevos modelos biomiméticos que permitan conocer mejor su evolución. Desarrollo. En esta revisión, actualizamos las plataformas y modelos más utilizados en los últimos años para estudiar la fisiopatología del ictus isquémico. Por un lado, repasamos las plataformas bi- y tridimensionales sobre las que se llevan a cabo los ensayos in vitro y, por otro lado, describimos los modelos experimentales in vivo más utilizados en la actualidad, así como las técnicas para evaluar el daño isquémico. Conclusiones. El desarrollo de buenos modelos experimentales tiene como fin último encontrar nuevas formas de tratamiento y, de esta manera, mejorar el pronóstico y la calidad de vida de los pacientes; por ello, es importante generar nuevos dispositivos in vitro y refinar más aún los modelos in vivo para hacer posible una buena traslación a la clínica.

Voltammetric behaviour and square-wave voltammetric determination of the potent antioxidant and anticarcinogenic agent ellagic acid in foodstuffs.

The voltammetric behaviour of ellagic acid (EA) is investigated by cyclic, differential pulse and square-wave voltammetry (CV, DPV and SWV, respectively). Based on the anodic oxidation peak at approximately 0.42V in acetic/acetate buffer (pH 5.5) a robust and a highly reliable square-wave voltammetric method is presented for the determination of EA. The oxidation peak current was linearly dependent on the concentration of EA in the range of 1.0×10(-7)-1.5×10(-6)mol/L (r=0.9997), with a detection limit of 1.0×10(-8)mol/L (S/N=3) and a quantification limit of 3.4×10(-8)mol/L (S/N=10), good reproducibility and a satisfactory level of selectivity towards others polyphenols. The proposed method was applied to the determination of free and total EA in fruits, nuts and juices with good analytical results being obtained.

Does Whole-Blood Neutrophil Gelatinase-Associated Lipocalin Stratify Acute Kidney Injury in Critically Ill Patients?

PURPOSE: To analyse the capacity of whole-blood NGAL (wbNGAL) to stratify AKI in critically ill patients with and without sepsis. METHODS: Whole-blood NGAL was measured with a point-of-care device at admission and 48 hours later in patients admitted to a general ICU. Patients were classified by the AKIN and KDIGO classifications at admission and 24 and 48 hours. We performed an ROC curve analysis. wbNGAL values at admission were compared in patients with sepsis and septic shock. RESULTS: The study included 100 consecutively admitted patients (40 female) with mean age 59.1 ± 17.8 years. Thirty-three patients presented AKI at admission, and 10 more developed it in the next 48 h. Eighteen patients had AKI stage 3, 14 of them at admission. Nine patients required renal replacement therapy. According to KDIGO at admission, wbNGAL values were 78 µg/L (60-187) in stage 0 (n = 67), 263 µg/L (89-314) in stage 1 (n = 8), 484 µg/L (333-708) in stage 2 (n = 11), and 623 µg/L (231-911) in stage 3 (n = 14), p = 0.0001 for trend. Ten patients did not complete 48 hours of study: 6 of 10 were discharged (initial wbNGAL 130 µg/L (60-514)) and 4 died (773 µg/L (311-1010)). The AUROC curve of wbNGAL to predict AKI was 0.838 (95% confidence interval 0.76-0.92, p = 0.0001), with optimal cut-off value of 178 µg/L (sensitivity 76.7%, specificity 78.9%, p < 0.0001). At admission, twenty-nine patients had sepsis, of whom 20 were in septic shock. wbNGAL concentrations were 81 µg/L (60-187) in patients without sepsis, 481 (247-687) in those with sepsis, and 623.5 µg/L (361-798) in the subgroup of septic shock (p < 0.0001). CONCLUSIONS: Whole-blood NGAL concentration at ICU admission was a good stratifier of AKI in critically ill patients. However, wbNGAL concentrations were higher in septic patients irrespective of AKI occurrence.

Cell-cycle arrest biomarkers in urine to predict acute kidney injury in septic and non-septic critically ill patients.

PURPOSE: To analyse the usefulness of the composite index of the tissue inhibitor of metalloproteinases-2 (TIMP-2) and insulin-like growth factor-binding protein 7 (IGFBP7) as urinary biomarkers for the early prediction of AKI in septic and non-septic patients. METHODS: This is a prospective, observational study including patients admitted to ICU from acute care departments and hospital length of stay <48 h. The main exclusion criteria were pre-existing eGFR <30 mL/min/1.73 m2 and hospitalisation 2 months prior to current admission. The [TIMP-2]·[IGFBP7] index was analysed twice, within the first 12 h of ICU admission. RESULTS: The sample included 98 patients. AKI incidence during ICU stay was 50%. Sepsis was diagnosed in 40.8%. Baseline renal variables were comparable between subgroups except for a higher baseline eGFR in non-septic patients. Patients were stratified based on the presence of AKI and their highest level of [TIMP-2]·[IGFBP7] within the first 12 h of stay. [TIMP-2]·[IGFBP7] index values were dependent on the incidence of AKI but not of sepsis. [TIMP-2]·[IGFBP7] values were significantly related to AKI severity according to AKIN criteria (p < 0.0001). The AUROC curve to predict AKI of the worst [TIMP-2]·[IGFBP7] index value was 0.798 (sensitivity 73.5%, specificity 71.4%, p < 0.0001). Index values below 0.8 ruled out any need for renal replacement (NPV 100%), whereas an index >0.8 predicted a rate of AKI of 71% and AKIN ≥ 2 of 62.9%. CONCLUSIONS: In our study, urinary [TIMP-2]·[IGFBP7] was an early predictor of AKI in ICU patients regardless of sepsis. Besides, index values <0.8(ng/mL)2/1000 ruled out the need for renal replacement.

Del laboratorio a la clínica en el ictus isquémico agudo. Modelos experimentales in vitro e in vivo / From the laboratory to the clinic in acute ischaemic stroke. In vitro and in vivo experimental models

Introducción: La enfermedad cerebrovascular es una de las principales causas de muerte, discapacidad y demencia en el mundo. La forma más frecuente de la enfermedad, el ictus isquémico, sólo tiene un fármaco disponible, el activador tisular del plasminógeno, y pocos pacientes pueden beneficiarse de esta terapia por los estrictos criterios de inclusión establecidos para su uso. Esta circunstancia hace crucial la búsqueda de nuevas formas de tratamiento para combatir las secuelas de la enfermedad, y para ello es necesario el desarrollo de nuevos modelos biomiméticos que permitan conocer mejor su evolución. Desarrollo: En esta revisión, actualizamos las plataformas y modelos más utilizados en los últimos años para estudiar la fisiopatología del ictus isquémico. Por un lado, repasamos las plataformas bi- y tridimensionales sobre las que se llevan a cabo los ensayos in vitro y, por otro lado, describimos los modelos experimentales in vivo más utilizados en la actualidad, así como las técnicas para evaluar el daño isquémico. Conclusiones: El desarrollo de buenos modelos experimentales tiene como fin último encontrar nuevas formas de tratamiento y, de esta manera, mejorar el pronóstico y la calidad de vida de los pacientes; por ello, es importante generar nuevos dispositivos in vitro y refinar más aún los modelos in vivo para hacer posible una buena traslación a la clínica.(AU)

Introduction: Cerebrovascular disease is one of the leading causes of death, disability and dementia around the world. For the most common form of the disease, ischaemic stroke, there is only one drug available, tissue plasminogen activator, and few patients can benefit from this therapy because of the strict inclusion criteria established for its use. This circumstance makes it crucial to search for new forms of treatment to combat the sequelae of the disease, and this requires the development of new biomimetic models that allow for a better understanding of its evolution. Development: In this review, we update the platforms and models most widely used in recent years to study the pathophysiology of ischaemic stroke. On the one hand, we review the two- and three-dimensional platforms on which in vitro assays are carried out and, on the other, we describe the most commonly used in vivo experimental models and techniques for assessing ischaemic damage. Conclusions: The ultimate aim of developing good experimental models is to find new forms of treatment and thus improve patients’ prognosis and quality of life. It is therefore important to generate new in vitro devices and to further refine in vivo models to enable a good clinical translation.(AU)

Specific Features of SVZ Neurogenesis After Cortical Ischemia: a Longitudinal Study.

Stroke is a devastating disease with an increasing prevalence. Part of the current development in stroke therapy is focused in the chronic phase, where neurorepair mechanisms such as neurogenesis, are involved. In the adult brain, one of the regions where neurogenesis takes place is the subventricular zone (SVZ) of the lateral ventricles. Given the possibility to develop pharmacological therapies to stimulate this process, we have performed a longitudinal analysis of neurogenesis in a model of cortical ischemia in mice. Our results show an initial decrease of SVZ proliferation at 24 h, followed by a recovery leading to an increase at 14d and a second decrease 28d after stroke. Coinciding with the 24 h proliferation decrease, an increase in the eutopic neuroblast migration towards the olfactory bulb was observed. The analysis of the neuroblast ectopic migration from the SVZ toward the lesion showed an increase in this process from day 14 after the insult. Finally, our data revealed an increased number of new cortical neurons in the peri-infarct cortex 65d after the insult. In summary, we report here critical check-points about post-stroke neurogenesis after cortical infarcts, important for the pharmacological modulation of this process in stroke patients.

Ovarian pure leiomyosarcoma: case report.

We report a case of a pure ovarian leiomyosarcoma, a rare tumor that comprises less than 0.1% out of all the ovarian malignant tumors.

[Erythroderma caused by carbamazepine. Diagnosis with skin patch]. / Eritrodermia por carbamacepina. Su diagnóstico mediante parche cutáneo.

We present two cases of cutaneous erythroderma induced by carbamazepine therapy, both cases with just cutaneous affection and only one suspicious drug. A cutaneous patch study, with standard battery from the Spanish Contact Dermatitis Research Group, vaseline with carbamazepine at 10% and lectures at 48 and 96 hours, was conducted. The result was positive for carbamazepine and negative for all other patches in both cases. All controls were negative. This is a very simple test, easy to perform, specific and with low side effects, allowing the diagnosis of this pathology.

Daidzein has neuroprotective effects through ligand-binding-independent PPARγ activation.

Phytoestrogens are a group of plant-derived compounds that include mainly isoflavones like daidzein. Phytoestrogens prevent neuronal damage and improve outcome in experimental stroke; however, the mechanisms of this neuroprotective action have not been fully elucidated. In this context, it has been postulated that phytoestrogens might activate the peroxisome proliferator-activated receptor-γ (PPARγ), which exerts neuroprotective effects in several settings. The aim of this study was to determine whether the phytoestrogen daidzein elicits beneficial actions in neuronal cells by mechanisms involving activation of PPARγ. Our results show that daidzein (0.05-5 µM) decreases cell death induced by exposure to oxygen-glucose deprivation (OGD) from rat cortical neurons and that improves synaptic function, in terms of increased synaptic vesicle recycling at nerve terminals, being both effects inhibited by the PPARγ antagonist T0070907 (1 µM). In addition, this phytoestrogen activated PPARγ in neuronal cultures, as shown by an increase in PPARγ transcriptional activity. Interestingly, these effects were not due to binding to the receptor ligand site, as shown by a TR-FRET PPARγ competitive binding assay. Conversely, daidzein increased PPARγ nuclear protein levels and decreased cytosolic ones, suggesting nuclear translocation. We have used the receptor antagonist (RE) fulvestrant to study the neuroprotective participation of daidzein via estrogen receptor and at least in our model, we have discarded this pathway. These results demonstrate that the phytoestrogen daidzein has cytoprotective properties in neurons, which are due to an increase in PPARγ activity not mediated by direct binding to the receptor ligand-binding domain but likely due to post-translational modifications affecting its subcellular location and not depending to the RE and it is not additive with the agonist rosiglitazone.

Benzodipyrrole derivates as new ionophores for anion-selective electrodes: improving potentiometric selectivity towards divalent anions.

Two open substituted benzodipyrroles were tested as hydrogen-bond-forming anion ionophores for the development of anion-selective electrodes. These compounds were incorporated in plasticized polymeric membranes with different plasticizers, using different membrane compositions to explore their response towards several anions. The electrodes constructed with membranes containing 2-nitrophenyl octyl ether and a 0.5 molar ratio ionic additive/ionophore showed pronounced anti-Hofmeister behaviour, providing a significantly enhanced response towards the divalent anions sulfate, sulfite, thiosulfate and oxalate. The selected electrodes were also evaluated in terms of detection limits and selectivity. (1)H NMR experiments were carried out in an attempt to explain some aspects of the behaviour observed.

Dopamine and α-synuclein dysfunction in Smad3 null mice.

BACKGROUND: Parkinson's disease (PD) is characterized by dopaminergic neurodegeneration in the substantia nigra (SN). Transforming growth factor-ß1 (TGF-ß1) levels increase in patients with PD, although the effects of this increment remain unclear. We have examined the mesostriatal system in adult mice deficient in Smad3, a molecule involved in the intracellular TGF-ß1 signalling cascade. RESULTS: Striatal monoamine oxidase (MAO)-mediated dopamine (DA) catabolism to 3,4-dihydroxyphenylacetic acid (DOPAC) is strongly increased, promoting oxidative stress that is reflected by an increase in glutathione levels. Fewer astrocytes are detected in the ventral midbrain (VM) and striatal matrix, suggesting decreased trophic support to dopaminergic neurons. The SN of these mice has dopaminergic neuronal degeneration in its rostral portion, and the pro-survival Erk1/2 signalling is diminished in nigra dopaminergic neurons, not associated with alterations to p-JNK or p-p38. Furthermore, inclusions of α-synuclein are evident in selected brain areas, both in the perikaryon (SN and paralemniscal nucleus) or neurites (motor and cingulate cortices, striatum and spinal cord). Interestingly, these α-synuclein deposits are detected with ubiquitin and P(S129)-α-synuclein in a core/halo cellular distribution, which resemble those observed in human Lewy bodies (LB). CONCLUSIONS: Smad3 deficiency promotes strong catabolism of DA in the striatum (ST), decrease trophic and astrocytic support to dopaminergic neurons and may induce α-synuclein aggregation, which may be related to early parkinsonism. These data underline a role for Smad3 in α-synuclein and DA homeostasis, and suggest that modulatory molecules of this signalling pathway should be evaluated as possible neuroprotective agents.

Utilización de las terapias de depuración extracorpórea en los Servicios de Medicina Intensiva de Cataluña (España) / Renal replacement therapy in Intensive Care Units in Catalonia (Spain)

OBJETIVOS: Conocer los tipos de terapias de depuración extracorpórea (TDE) utilizadas en los Servicios de Medicina Intensiva (SMI), sus indicaciones y pautas de prescripción. DISEÑO: Estudio multicéntrico observacional y prospectivo. ÁMBITO: Servicios de Medicina Intensiva. PACIENTES: Todos los pacientes ingresados en los SMI que requirieron TDE durante 2 meses en 2011.Intervenciones Ninguna.VARIABLES DE INTERÉS: Características demográficas y basales de los pacientes, características de las TDE y materiales utilizados. RESULTADOS: Se analizó a 33 pacientes. Las TDE se iniciaron en las primeras 24 h de ingreso en un 52% (n = 17). En un 18% (n = 6) de pacientes se inició en el estadio R de disfunción renal aguda (DRA) según el RIFLE. La patología más frecuente asociada a la DRA fue el síndrome de disfunción multiorgánica en un 64% (n = 21). El 24% (n = 8) mantenía estabilidad hemodinámica al inicio de la TDE y el tipo de terapia más utilizada en estos pacientes fueron las terapias continuas de depuración extracorpórea (TCDE) en un 63% (n = 5). El 76% (n = 25) de los pacientes presentaron inestabilidad hemodinámica y en todos la terapia utilizada fue la TCDE. Se utilizó anticoagulación en un 55% (n = 18) de casos y la vía de acceso preferida fue la femoral derecha en un 61% (n = 20). En el 84% (n = 28) de los pacientes se utilizó una dosis pautada de ultrafiltración ≤ 35 ml/kg/h. CONCLUSIONES: Los SMI estudiados siguen las recomendaciones actuales del uso de las TDE. Existe una mayor preferencia de las terapias continuas frente a las intermitentes, indistintamente al estado hemodinámico del paciente

OBJECTIVE: To assess the indications, settings and techniques used in renal replacement therapy (RRT) in Intensive Care Units (ICUs). STUDY DESIGN: A prospective, multicenter observational study was carried out. SETTING: Intensive Care Units. PATIENTS: All patients admitted to ICUs during the two-month study period in 2011 who required RRT. Interventions None. VARIABLES OF INTEREST: Patient demographic characteristics, baseline clinical data, RRT technique and materials used. RESULTS: Thirty-three patients were analyzed. RRT was started within the first 24hours after ICU admission in 17 of the 33 patients (52%). At the start of RRT, 18% of the patients (n = 6) presented grade R on the RIFLE acute kidney injury (AKI) scale. The most common disorder associated with AKI was multiple organ dysfunction syndrome (64%; n = 21). At the start of RRT, most patients (76%; n = 25) presented hemodynamic instability, while the remaining 24% (n = 8) were considered hemodynamically stable. The most common RRT technique in hemodynamically stable patients was continuous renal replacement therapy (CRRT) (63%; n = 5). CRRT was the technique of choice in all 25 of the hemodynamically unstable patients (100%). Anticoagulation was used in 55% (n = 18) of the patients. In most cases (61%, n = 20), RRT was administered through the right femoral vein. In 84% (n = 28) of the patients, the ultrafiltration effluent flow rate was ≤ 35 ml/kg/h. CONCLUSIONS: The ICU physicians in this study followed current RRT guidelines. CRRT was preferred over intermittent renal replacement therapy, regardless of patient hemodynamic status