Description of gasket failure in a 7 cell PEMFC stack

This article presents the data and the description of a fuel cell stack that failed due to gasket degradation. The fuel cell under study is a 7 cell stack. The unexpected change in several variables such as temperature, pressure and voltage indicated the possible failure of the stack. The stack was monitored over a 6 h period in which data was collected and consequently analyzed to conclude that the fuel cell stack failed due to a crossover leak on the anode inlet port located on the cathode side gasket of cell #2. This stack failure analysis revealed a series of indicators that could be used by a super visional controller in order to initiate a shutdown procedure.Instituto de Investigaciones en Electrónica, Control y Procesamiento de Señale

Brain-derived neurotrophic factor (BDNF) and polysialylated-neural cell adhesion molecule (PSA-NCAM) in the human brainstem precerebellar nuclei from prenatal to adult age.

Occurrence and distribution of the neurotrophin brain-derived neurotrophic factor (BDNF) and polysialylated-neural cell adhesion molecule (PSA-NCAM), a neuroplasticity marker known to modulate BDNF signalling, were examined by immunohistochemistry in the human brainstem precerebellar nuclei at prenatal, perinatal and adult age. Western blot analysis performed in human brainstem showed for both molecules a single protein band compatible with the molecular weight of the dimeric form of mature BDNF and with that of PSA-NCAM. Detectability of both molecules up to 72 h post-mortem was also assessed in rat brain. In neuronal perikarya, BDNF-like immunoreactivity (LI) appeared as intracytoplasmic granules, whereas PSA-NCAM-LI appeared mostly as peripheral staining, indicative of membrane labelling; immunoreactivity to both substances also labelled nerve fibres and terminals. BDNF- and PSA-NCAM-LI occurred in the external cuneate nucleus, perihypoglossal nuclei, inferior olive complex, arcuate nucleus, lateral reticular formation, vestibular nuclei, pontine reticulotegmental and paramedian reticular nuclei, and pontine basilar nuclei. With few exceptions, for both substances the distribution pattern detected at prenatal age persisted later on, though the immunoreactivity appeared often higher in preand full-term newborns than in adult specimens. The results obtained suggest that BDNF operates in the development, maturation, maintenance and plasticity of human brainstem precerebellar neuronal systems. They also imply a multiple origin for the BDNF-LI of the human cerebellum. The codistribution of BDNF- and PSA-NCAM-LI in analyzed regions suggests that PSA-NCAM may modulate the functional interaction between BDNF and its high and low affinity receptors, an issue worth further analysis, particularly in view of the possible clinical significance of neuronal trophism in cerebellar neurodegenerative disorders.

Anti-Inflammatory Effect of Beta-Caryophyllene Mediated by the Involvement of TRPV1, BDNF and trkB in the Rat Cerebral Cortex after Hypoperfusion/Reperfusion

We have previously shown that bilateral common carotid artery occlusion followed by reperfusion (BCCAO/R) is a model to study early hypoperfusion/reperfusion-induced changes in biomarkers of the tissue physiological response to oxidative stress and inflammation. Thus in this study, we investigate with immunochemical assays if a single dose of beta-caryophyllene (BCP), administered before the BCCAO/R, can modulate the TRPV1, BDNF, and trkB receptor in the brain cortex; the glial markers GFAP and Iba1 were also examined. Frontal and temporal-occipital cortical regions were analyzed in two groups of male rats, sham-operated and submitted to BCCAO/R. Six hours before surgery, one group was gavage fed a dose of BCP (40 mg/per rat in 300 mu L of sunflower oil), the other was pre-treated with the vehicle alone. Western blot analysis showed that, in the frontal cortex of vehicle-treated rats, the BCCAO/R caused a TRPV1 decrease, an increment of trkB and GFAP, no change in BDNF and Iba1. The BCP treatment caused a decrease of BDNF and an increase of trkB levels in both sham and BCCAO/R conditions while inducing opposite changes in the case of TRPV1, whose levels became higher in BCCAO/R and lower in sham conditions. Present results highlight the role of BCP in modulating early events of the cerebral inflammation triggered by the BCCAO/R through the regulation of TRPV1 and the BDNF-trkB system

Effects of forced swimming stress on ERK and histone H3 phosphorylation in limbic areas of Roman high-and low-avoidance rats

Stressful events evoke molecular adaptations of neural circuits through chromatin remodeling and regulation of gene expression. However, the identity of the molecular pathways activated by stress in experimental models of depression is not fully understood. We investigated the effect of acute forced swimming (FS) on the phosphorylation of the extracellular signal-regulated kinase (ERK)1/2 (pERK) and histone H3 (pH3) in limbic brain areas of genetic models of vulnerability (RLA, Roman low-avoidance rats) and resistance (RHA, Roman high-avoidance rats) to stress-induced depression-like behavior. We demonstrate that FS markedly increased the density of pERK-positive neurons in the infralimbic (ILCx) and the prelimbic area (PrLCx) of the prefrontal cortex (PFCx), the nucleus accumbens, and the dorsal blade of the hippocampal dentate gyrus to the same extent in RLA and RHA rats. In addition, FS induced a significant increase in the intensity of pERK immunoreactivity (IR) in neurons of the PFCx in both rat lines. However, RHA rats showed stronger pERK-IR than RLA rats in the ILCx both under basal and stressed conditions. Moreover, the density of pH3-positive neurons was equally increased by FS in the PFCx of both rat lines. Interestingly, pH3-IR was higher in RHA than RLA rats in PrLCx and ILCx, either under basal conditions or upon FS. Finally, colocalization analysis showed that in the PFCx of both rat lines, almost all pERK-positive cells express pH3, whereas only 50% of the pH3-positive neurons is also pERK-positive. Moreover, FS increased the percentage of neurons that express exclusively pH3, but reduced the percentage of cells expressing exclusively pERK. These results suggest that (i) the distinctive patterns of FS-induced ERK and H3 phosphorylation in the PFCx of RHA and RLA rats may represent molecular signatures of the behavioural traits that distinguish the two lines and (ii) FS-induced H3 phosphorylation is, at least in part, ERK-independent

Successful Treatment of Chronic Mucocutaneous Candidiasis Caused by Azole-Resistant Candida albicans with Posaconazole

Refractory or recurrent infections of skin, nails, and the mucous membranes are clinical signs of chronic mucocutaneous candidiasis, frequently associated with immunological defects. Here we describe a 39-years-old female patient, with familial CMC, that presented with an extensive infection caused by an azole-resistant Candida albicans isolate, successfully treated with posaconazole

Binge-like administration of alcohol mixed to energy drinks to male adolescent rats severely impacts on mesocortical dopaminergic function in adulthood: A behavioral, neurochemical and electrophysiological study

A growing body of evidence indicates that the practice of consuming alcohol mixed with energy drinks (ED) (AMED) in a binge drinking pattern is significantly diffusing among the adolescent population. This behavior, aimed at increasing the intake of alcohol, raises serious concerns about its long-term effects. Epidemiological studies suggest that AMED consumption might increase vulnerability to alcohol abuse and have a gating effect on the use of illicit drugs. The medial prefrontal cortex (mPFC) is involved in the modulation of the reinforcing effects of alcohol and of impulsive behavior and plays a key role in the development of addiction. In our study, we used a binge-like protocol of administration of alcohol, ED, or AMED in male adolescent rats, to mimic the binge-like intake behavior observed in humans, in order to evaluate whether these treatments could differentially affect the function of mesocortical dopaminergic neurons in adulthood. We did so by measuring: i) physiological sensorimotor gating; ii) voluntary alcohol consumption and dopamine transmission before, during, and after presentation of alcohol; iii) electrophysiological activity of VTA dopaminergic neurons and their sensitivity to a challenge with alcohol. Our results indicate that exposure to alcohol, ED, or AMED during adolescence induces differential adaptive changes in the function of mesocortical dopaminergic neurons and, in particular, that AMED exposure decreases their sensitivity to external stimuli, possibly laying the foundation for the altered behaviors observed in adulthood

Neuroplastic changes in c-Fos, ΔFosB, BDNF, trkB, and Arc expression in the hippocampus of male Roman rats: differential effects of sexual activity

Sexual activity causes differential changes in the expression of markers of neural activation (c-Fos and Delta FosB) and neural plasticity (Arc and BDNF/trkB), as determined either by Western Blot (BDNF, trkB, Arc, and Delta FosB) or immunohistochemistry (BDNF, trkB, Arc, and c-Fos), in the hippocam pus of male Roman high (RHA) and low avoidance (RLA) rats, two psychogenetically selected rat lines that display marked differences in sexual behavior (RHA rats exhibit higher sexual motivation and better copulatory performance than RLA rats). Both methods showed (with some differences) that sexual activity modifies the expression levels of these markers in the hippocampus of Roman rats depending on: (i) the level of sexual experience, that is, changes were usually more evident in sexually naive than in experienced rats; (ii) the hippocampal partition, that is, BDNF and Arc increased in the dorsal but tended to decrease in the ventral hippocampus; (iii) the marker considered, that is, in sexually experienced animals BDNF, c-Fos, and Arc levels were similar to those of controls, while Delta FosB levels increased; and (iv) the rat line, that is, changes were usually larger in RHA than RLA rats. These findings resemble those of early studies in RHA and RLA rats showing that sexual activity influences the expression of these markers in the nucleus accumbens, medial prefrontal cortex, and ventral tegmental area, and show for the first time that also in the hippocampus sexual activity induces neural activation and plasticity, events that occur mainly during the first phase of the acquisition of sexual experience and depend on the genotypic/phenotypic characteristics of the animals

BDNF, trkB and PSA-NCAM in the hippocampus of Roman rats after forced swimming

The selective breeding of Roman High- (RHA) and Low-Avoidance (RLA) rats are considered as a genetic model of resilience to stress-induced depression and of vulnerability to that trait, respectively1. There is evidence that alterations in neuronal plasticity in the hippocampus and other brain areas are critically involved in the pathophysiology of mood disorders. Here, we investigated on immunochemical occurrence of Brain-derived neurotrophic factor (BDNF), tyrosine-kinase receptor trkB and polysialilated form of the neural cell adhesion molecule (PSANCAM) in the hippocampus of the Roman rat lines under baseline conditions and after acute forced swimming (FS). Western blot (WB) analyses showed that, in basal conditions, the relative levels of BDNF, trkB and PSA-NCAM markedly differed, appearing lower by 48%, 25% and 65%, respectively, in RLA vs RHA rats. WB analyses carried out after FST showed no differences between baseline and FST rats. In tissue sections, BDNF-, trkB- and PSA-NCAM-like immunoreactivity (LI) showed a distinctive labelling, mainly localized to proximal neuronal processes and nerve fibers distributed in the Ammon’s horn and dentate gyrus (DG). A number of PSA-NCAM-positive neurons in the subgranular layer of dentate gyrus also occurred. Densitometric analysis further showed differences in the hippocampal subregions. Thus, upon FST, BDNF-LI was less abundant in the CA3 sector of the Ammon’s horn of FST vs control RLA rats (-24%), whereas PSA-NCAM-LI was more abundant in the DG of RHA than RLA rats (+26%). Our findings suggest that an altered neuronal availability of and/or responsiveness to BDNF and inadequate dynamic events related to neuroplasticity may contribute to outline the molecular and morphological basis for the distinct vulnerability to stress-induced depression in the two rat lines

Immunochemical detection of trkB receptor in the brain of a rat model of depression

The outbread Roman High- (RHA) and Roman Low-Avoidance (RLA) rat lines were psychogenetically selected for rapid versus poor acquisition of active avoidance, respectively, and differ in many behavioural traits that closely resemble the cardinal symptoms of depression (1). Beyond the monoamine hypothesis of depression, compelling evidence suggests that mood disorders are characterized by reduced neuronal plasticity. Consistently, it has been shown that exposure to stress and antidepressant treatment modulate the expression of neurotrophic molecules and their relevant receptors, and that these changes show an anatomical specificity (2). With the aim to characterize the molecular and neuronal systems involved in the pathogenesis of depression and in the mechanism of action of the antidepressant treatments, here we investigate on the immunochemical occurrence of trkB, the high affinity tyrosinekinase receptor for brain-derived neurotrophic factor (BDNF), in selected areas of the RHA and RLA rat brain by means of western blot (WB) and immunohistochemistry. WB analysis indicates that the relative levels of trkB patently and markedly differed in the prefrontal cortex and the hippocampus, where they were lower in RLA vs RHA rats, and in the caudate-putamen complex proper where, by contrast, they were higher in RLA vs RHA rats. No statistically significant differences were seen in nucleus accumbens and ventral tegmental area. In tissue sections, trkB-like immunoreactive (LI) labelling was mainly localized to neuronal cell bodies and proximal processes, unevenly distributed in the telencephalic cerebral cortex, the hippocampus, and the ventral tegmentum of the midbrain. Densitometric analysis of immunostained brain sections revealed that differences among the two groups are consistent to a good extent with WB data. As a whole, the finding of a different expression of trkB receptor in the RLA vs RHA rat brains implies the occurrence of an altered neuronal responsiveness to BDNF in specific brain regions and may contribute to outline the molecular and morphological basis for the distinct vulnerability to depression in the two rat lines