23 research outputs found

    Differential Stress-Induced Neuronal Activation Patterns in Mouse Lines Selectively Bred for High, Normal or Low Anxiety

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    There is evidence for a disturbed perception and processing of emotional information in pathological anxiety. Using a rat model of trait anxiety generated by selective breeding, we previously revealed differences in challenge-induced neuronal activation in fear/anxiety-related brain areas between high (HAB) and low (LAB) anxiety rats. To confirm whether findings generalize to other species, we used the corresponding HAB/LAB mouse model and investigated c-Fos responses to elevated open arm exposure. Moreover, for the first time we included normal anxiety mice (NAB) for comparison. The results confirm that HAB mice show hyperanxious behavior compared to their LAB counterparts, with NAB mice displaying an intermediate anxiety phenotype. Open arm challenge revealed altered c-Fos response in prefrontal-cortical, limbic and hypothalamic areas in HAB mice as compared to LAB mice, and this was similar to the differences observed previously in the HAB/LAB rat lines. In mice, however, additional differential c-Fos response was observed in subregions of the amygdala, hypothalamus, nucleus accumbens, midbrain and pons. Most of these differences were also seen between HAB and NAB mice, indicating that it is predominately the HAB line showing altered neuronal processing. Hypothalamic hypoactivation detected in LAB versus NAB mice may be associated with their low-anxiety/high-novelty-seeking phenotype. The detection of similarly disturbed activation patterns in a key set of anxiety-related brain areas in two independent models reflecting psychopathological states of trait anxiety confirms the notion that the altered brain activation in HAB animals is indeed characteristic of enhanced (pathological) anxiety, providing information for potential targets of therapeutic intervention

    Dendritic Morphology of Hippocampal and Amygdalar Neurons in Adolescent Mice Is Resilient to Genetic Differences in Stress Reactivity

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    Many studies have shown that chronic stress or corticosterone over-exposure in rodents leads to extensive dendritic remodeling, particularly of principal neurons in the CA3 hippocampal area and the basolateral amygdala. We here investigated to what extent genetic predisposition of mice to high versus low stress reactivity, achieved through selective breeding of CD-1 mice, is also associated with structural plasticity in Golgi-stained neurons. Earlier, it was shown that the highly stress reactive (HR) compared to the intermediate (IR) and low (LR) stress reactive mice line presents a phenotype, with respect to neuroendocrine parameters, sleep architecture, emotional behavior and cognition, that recapitulates some of the features observed in patients suffering from major depression. In late adolescent males of the HR, IR, and LR mouse lines, we observed no significant differences in total dendritic length, number of branch points and branch tips, summated tip order, number of primary dendrites or dendritic complexity of either CA3 pyramidal neurons (apical as well as basal dendrites) or principal neurons in the basolateral amygdala. Apical dendrites of CA1 pyramidal neurons were also unaffected by the differences in stress reactivity of the animals; marginally higher length and complexity of the basal dendrites were found in LR compared to IR but not HR mice. In the same CA1 pyramidal neurons, spine density of distal apical tertiary dendrites was significantly higher in LR compared to IR or HR animals. We tentatively conclude that the dendritic complexity of principal hippocampal and amygdala neurons is remarkably stable in the light of a genetic predisposition to high versus low stress reactivity, while spine density seems more plastic. The latter possibly contributes to the behavioral phenotype of LR versus HR animals

    Recording and playback of video signals with support for multiple cameras based on FPGAs

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    Zadatak ovog diplomskog rada je napraviti FPGA dizajn koji omogućava AMV Grabber ploči primanje i zapisivanje podataka s kamera, te slanje već snimljenog video sadržaja na izlazne portove. AMV Grabber ploča ima ulogu produžetka ADAS (engl. Advanced Driver Assistance System) uređaja, jer AMV Grabber omogućava lakši razvoj i testiranje ADAS algoritama. Dizajniranje je odrađeno u Xilinx®-ovom okruženju Vivado®, te su korišteni službeni IP blokovi koje regulira Xilinx®. Rješenje je razdvojeno na dva dijela, putanja snimanja i putanja reprodukcije iz razloga što nije bilo moguće putanju reprodukcije implementirati u kompletan projekt. Omogućeno je snimanje do devet kamera, iako hardverska ograničenja nisu dozvoljavala dovoljan protok podataka, usko grlo se pojavilo pri zapisivanju podataka na tvrdi disk. Putanja reprodukcije je razvijena zasebno i potvrda njene funkcionalnosti zahtijevala je pozamašna testiranja. Ispostavilo se da je slanje moguće, uz mali gubitak pet početnih okvira koje je nemoguće sačuvati jer su potrebni za sinkronizaciju blokova u dizajnu reprodukcije.The purpose of this master thesis is to create an FPGA design, which allows capturing data from cameras, and reproduction of already captured data to the output ports on AMV Grabber device. AMV Grabber device acts as an extension of ADAS (Advanced Driver Assistance Systems) which allows easier development and testing of ADAS algorithms. The design has been made in Vivavo® design suite by Xilinx®. For the purposes of the design official IPs have been used. Developed design is separated into two parts, input path, and output path, because output path was not possible to implement into the complete project. Input path is able to record with up to nine cameras, even though only theoretically. Actual capabilities were the recording with five cameras because there happened to be a data flow bottle neck when writing on the SSD drive, and no AMV Grabber device had all nine input ports functional. Output path was developed on its own, so the verification of requested behavior was extensive. The final result was successful reproduction of test data with first five frame loss, due to synchronization process of the IPs used in the output design

    Interaction of red blood cells with arrays of laser-induced cavitation bubbles

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    We use a spatial light modulator (SLM) to simultaneously create several laser-induced cavitation bubbles. The geometry o the bubble array results in different flow patterns during the expansion and collapse of the bubbles. Hence, the induced shear stresses that affect cells are also modified by the geometry. The events are imaged using strobe photography and high speed cameras. In particular we study the deformability of red blood cells due to the shear stresses, since RBC deformability is a potential indicator for several diseases including malaria [1]

    Health-related quality of life and distress in elderly vs. younger patients with high-grade glioma—results of a multicenter study

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    Objective!#!Half of all newly diagnosed patients with glioblastoma are > 65 years still with a poor prognosis. Preserving quality of life is of high importance. However, patient reported outcome (PRO) data in this patient group is rare. The aim was to compare health-related quality of life (HRQoL) and distress between elderly and younger patients with high-grade glioma (HGG).!##!Methods!#!We used baseline data of a prospective study where HGG patients were enrolled from 4 hospitals. Distress was measured using the distress thermometer (DT), HRQoL using the European Organization for Research and Treatment of Cancer (EORTC) Quality of Life Core Questionnaire (QLQ-C30) plus brain module (BN20). We compared distress and HRQoL by age (≥ 65 vs. < 65 years), gender, performance score, and time since diagnosis using multivariate linear and logistic regressions.!##!Results!#!A total of n = 93 (30%) out of n = 309 patients were ≥ 65 years (mean 70 years, range 65-86 years). Mean DT score of elderly patients (5.2, SD 2.6) was comparable with younger patients (4.9, SD 2.6). Elderly patients reported significantly lower global health (GHS, mean elderly vs. younger; 50.8 vs. 60.5, p = 0.003), worse physical (56.8 vs. 73.3, p < 0.001) and lower cognitive functioning (51.1 vs. 63.2, p = 0.002), worse fatigue (52.5 vs. 43.5, p = 0.042), and worse motor dysfunction (34.9 vs. 23.6, p = 0.030). KPS and not age was consistently associated with HRQoL.!##!Conclusion!#!Physical functioning was significantly reduced in the elderly compared with younger HGG patients, and at the same time, emotional functioning and DT scores were comparable. KPS shows a greater association with HRQoL than with calendric age in HGG patients reflecting the particular importance for adequate assessment of HRQoL and general condition in elderly patients

    The p38-Mediated Rapid Down-Regulation of Cell Surface gp130 Expression Impairs Interleukin-6 Signaling in the Synovial Fluid of Juvenile Idiopathic Arthritis Patients

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    Objective. Interleukin-6 (IL-6) signaling plays an important proinflammatory role, but this role is restricted by regulatory mechanisms that, for example, reduce the cell surface availability of the signaltransducing chain of the IL-6 receptor, gp130. The aim of this study was to determine whether the inflammatory environment in arthritic joints has an impact on monocytic gp130 surface expression and the extent to which regulatory processes in the synovial fluid (SF) can be reproduced in an in vitro model. Methods. Flow cytometry and live cell imaging were used to measure the cell surface expression and internalization of gp130. STAT-3 phosphorylation was monitored by flow cytometry and Western blotting. Results. In patients with juvenile idiopathic arthritis (JIA), levels of cell surface gp130 expression in SF monocytes were reduced compared to those in peripheral blood (PB) monocytes. These reduced levels were reproduced when PB monocytes from healthy donors were stim ulated with SF, and this reduction was dependent on p38 MAPK. The induction of p38 by IL-1 in PB monocytes interfered with IL-6 signaling due to the reduced cell surface expression of gp130. Conclusion. These results suggest that p38- mediated proinflammatory stimuli induce the downregulation of gp130 on monocytes and thus restrict gp130-mediated signal transduction. This regulatory mechanism could be of relevance to processes in the inflamed joints of patients with JIA
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