Dynamic Optical Tweezers using Acousto-Optic Modulators

Treballs Finals de Grau de Física, Facultat de Física, Universitat de Barcelona, Any: 2015, Tutors: Estela Martín Badosa i Mario Montes UsateguiThis work consists of the study, characterisation and set-up of an Acousto-Optic Light Modulator made up of two TeO2 crystals, to use it in an optical tweezers system. We have performed the following tasks: optical system assembly and alignment, optimization of the first diffraction order efficiency of the device and, finally, deflection analysis. Furthermore, we have developed a control system based on a multi-function data acquisition board and a software using LabVIEW that allows the user to dynamically control the position of the laser spot, as well as its amplitude. Lastly, we have improved the program making possible the use of time-sharing trapping

A follow-me algorithm for AR.Drone using MobileNet-SSD and PID control

Treballs Finals de Grau d'Enginyeria Informàtica, Facultat de Matemàtiques, Universitat de Barcelona, Any: 2018, Director: Lluís Garrido Ostermann[en] In recent years the industry of quadcopters has experimented a boost. The appearance of inexpensive drones has led to the growth of the recreational use of this vehicles, which opens the door to the creation of new applications and technologies. This thesis presents a vision-based autonomous control system for an AR.Drone 2.0. A tracking algorithm is developed using onboard vision systems without relying on additional external inputs. In particular, the tracking algorithm is the combination of a trained MobileNet-SSD object detector and a KCF tracker. The noise induced by the tracker is decreased with a Kalman filter. Furthermore, PID controllers are implemented for the motion control of the quadcopter, which process the output of the tracking algorithm to move the drone to the desired position. The final implementation was tested indoors and the system yields acceptable results

Poor sleep is associated with deficits of attention in COPD patients

COPD; Cognitive impairment; SleepEPOC; Deterioro cognitivo; DormirMPOC; Discapacitat cognitiva; DormirBackground Poor sleep and attention deficits are common in COPD. Objectives To assess the relationship between self-reported poor sleep and attention deficits in COPD. We also studied the association between self-reported sleep and the attention tests with the objective characteristics of sleep. Methods Fifty-nine COPD patients were prospectively studied. Self-reported sleep quality was assessed using the Pittsburgh sleep quality index (PSQI). Objective characteristics of sleep were assessed by actigraphy and polysomnography. Attention was evaluated with the Oxford sleep resistance test (OSLER) and the Psychomotor vigilance test (PVT). Results 28 (47 %) patients referred poor sleep (PSQI >5). In the OSLER test they showed earlier sleep onset than patients with good sleep, median (Interquartil range): 31.2 min (25.4–40) vs 40 min (28.5–40), p: 0.048. They also spent more time making errors: 4.5 % (0.6–7.6) of total test time vs 0.7 % (0.2–5.3), p: 0.048. In PVT, patients with poor sleep presented a greater dispersion of the reaction time values with a higher value in the slowest 10 % of the reactions, 828 (609–1667) msec. vs 708 (601–993) msec, p: 0.028. No association was found between self-reported poor sleep and objective sleep variables. We found no correlation between OSLER and PVT results and polysomnographic variables except between sleep efficiency and PVT response speed (β: 0.309, p: 0.018). Conclusion Self-reported poor sleep in COPD is associated with attention deficits. Sleep quality should be included in future studies of this facet of cognition in COPD, as well as to assess its potential usefulness as a therapeutic target.This study was funded by AstraZeneca Spain

Cognitive Decline and BPSD Are Concomitant with Autophagic and Synaptic Deficits Associated with G9a Alterations in Aged SAMP8 Mice

Behavioural and psychological symptoms of dementia (BPSD) are presented in 95% of Alzheimer's Disease (AD) patients and are also associated with neurotrophin deficits. The molecular mechanisms leading to age-related diseases are still unclear; however, emerging evidence has suggested that epigenetic modulation is a key pathophysiological basis of ageing and neurodegeneration. In particular, it has been suggested that G9a methyltransferase and its repressive histone mark (H3K9me2) are important in shaping learning and memory by modulating autophagic activity and synaptic plasticity. This work deepens our understanding of the epigenetic mechanisms underlying the loss of cognitive function and BPSD in AD. For this purpose, several tasks were performed to evaluate the parameters of sociability (three-chamber test), aggressiveness (resident intruder), anxiety (elevated plus maze and open field) and memory (novel object recognition test) in mice, followed by the evaluation of epigenetic, autophagy and synaptic plasticity markers at the molecular level. The behavioural alterations presented by senescence-accelerated mice prone 8 (SAMP8) of 12 months of age compared with their senescence-accelerated mouse resistant mice (SAMR1), the healthy control strain was accompanied by age-related cognitive deficits and alterations in epigenetic markers. Increased levels of G9a are concomitant to the dysregulation of the JNK pathway in aged SAMP8, driving a failure in autophagosome formation. Furthermore, lower expression of the genes involved in the memory-consolidation process modulated by ERK was observed in the aged male SAMP8 model, suggesting the implication of G9a. In any case, two of the most important neurotrophins, namely brain-derived neurotrophic factor (Bdnf) and neurotrophin-3 (NT3), were found to be reduced, along with a decrease in the levels of dendritic branching and spine density presented by SAMP8 mice. Thus, the present study characterizes and provides information regarding the non-cognitive and cognitive states, as well as molecular alterations, in aged SAMP8, demonstrating the AD-like symptoms presented by this model. In any case, our results indicate that higher levels of G9a are associated with autophagic deficits and alterations in synaptic plasticity, which could further explain the BPSD and cognitive decline exhibited by the model

A Combined Chronic Low-Dose Soluble Epoxide Hydrolase and Acetylcholinesterase Pharmacological Inhibition Promotes Memory Reinstatement in Alzheimer's Disease Mice Models

Alzheimer's disease (AD) is a progressive neurological disorder with multifactorial and heterogeneous causes. AD involves several etiopathogenic mechanisms such as aberrant protein accumulation, neurotransmitter deficits, synaptic dysfunction and neuroinflammation, which lead to cognitive decline. Unfortunately, the currently available anti-AD drugs only alleviate the symptoms temporarily and provide a limited therapeutic effect. Thus, new therapeutic strategies, including multitarget approaches, are urgently needed. It has been demonstrated that a co-treatment of acetylcholinesterase (AChE) inhibitor with other neuroprotective agents has beneficial effects on cognition. Here, we have assessed the neuroprotective effects of chronic dual treatment with a soluble epoxide hydrolase (sEH) inhibitor (TPPU) and an AChE inhibitor (6-chlorotacrine or rivastigmine) in in vivo studies. Interestingly, we have found beneficial effects after chronic low-dose co-treatment with TPPU and 6-chlorotacrine in the senescence-accelerated mouse prone 8 (SAMP8) mouse model as well as with TPPU and rivastigmine co-treatment in the 5XFAD mouse model, in comparison with the corresponding monotherapy treatments. In the SAMP8 model, no substantial improvements in synaptic plasticity markers were found, but the co-treatment of TPPU and 6-chlorotacrine led to a significantly reduced gene expression of neuroinflammatory markers, such as interleukin 6 (Il-6), triggering receptor expressed on myeloid cell 2 (Trem2) and glial fibrillary acidic protein (Gfap). In 5XFAD mice, chronic low-dose co-treatment of TPPU and rivastigmine led to enhanced protein levels of synaptic plasticity markers, such as the phospho-cAMP response element-binding protein (p- CREB) ratio, brain-derived neurotrophic factor (BDNF) and postsynaptic density protein 95 (PSD95), and also to a reduction in neuroinflammatory gene expression. Collectively, these results support the neuroprotectant role of chronic low-dose co-treatment strategy with sEH and AChE inhibitors in AD mouse models, opening new avenues for effective AD treatment

Dynamics of Gene Expression Profiling and Identification of High-Risk Patients for Severe COVID-19

The clinical manifestations of SARS-CoV-2 infection vary widely, from asymptomatic infection to the development of acute respiratory distress syndrome (ARDS) and death. The host response elicited by SARS-CoV-2 plays a key role in determining the clinical outcome. We hypothesized that determining the dynamic whole blood transcriptomic profile of hospitalized adult COVID-19 patients and characterizing the subgroup that develops severe disease and ARDS would broaden our understanding of the heterogeneity in clinical outcomes. We recruited 60 hospitalized patients with RT-PCR-confirmed SARS-CoV-2 infection, among whom 19 developed ARDS. Peripheral blood was collected using PAXGene RNA tubes within 24 h of admission and on day 7. There were 2572 differently expressed genes in patients with ARDS at baseline and 1149 at day 7. We found a dysregulated inflammatory response in COVID-19 ARDS patients, with an increased expression of genes related to pro-inflammatory molecules and neutrophil and macrophage activation at admission, in addition to an immune regulation loss. This led, in turn, to a higher expression of genes related to reactive oxygen species, protein polyubiquitination, and metalloproteinases in the latter stages. Some of the most significant differences in gene expression found between patients with and without ARDS corresponded to long non-coding RNA involved in epigenetic control

Deletion of Gadd45a Expression in Mice Leads to Cognitive and Synaptic Impairment Associated with Alzheimer’s Disease Hallmarks.

Gadd45 genes have been implicated in survival mechanisms, including apoptosis, autophagy,cell cycle arrest, and DNA repair, which are processes related to aging and life span. Here, weanalyzed if the deletion of Gadd45a activates pathways involved in neurodegenerative disorders suchas Alzheimer’s Disease (AD). This study used wild-type (WT) and Gadd45a knockout (Gadd45a−/−)mice to evaluate AD progression. Behavioral tests showed that Gadd45a−/− mice presented lowerworking and spatial memory, pointing out an apparent cognitive impairment compared with WTanimals, accompanied by an increase in Tau hyperphosphorylation and the levels of kinases involvedin its phosphorylation in the hippocampus. Moreover, Gadd45a−/− animals significantly increased thebrain’s pro-inflammatory cytokines and modified autophagy markers. Notably, neurotrophins andthe dendritic spine length of the neurons were reduced in Gadd45a−/− mice, which could contributeto the cognitive alterations observed in these animals. Overall, these findings demonstrate that thelack of the Gadd45a gene activates several pathways that exacerbate AD pathology, suggesting thatpromoting this protein’s expression or function might be a promising therapeutic strategy to slowdown AD progression.</p

Las personas sordas en comunidades orales bilingües : el caso de las personas sordas en Barcelona

Versión española de "Deaf people in bilingual speaking communities: The case of Deaf People in Barcelona

Particle size and cholesterol content of circulating HDL correlate with cardiovascular death in chronic heart failure

Evidence regarding any association of HDL-particle (HDL-P) derangements and HDL-cholesterol content with cardiovascular (CV) death in chronic heart failure (HF) is lacking. To investigate the prognostic value of HDL-P size (HDL-Sz) and the number of cholesterol molecules per HDL-P for CV death in HF patients. Outpatient chronic HF patients were enrolled. Baseline HDL-P number, subfractions and HDL-Sz were measured using 1H-NMR spectroscopy. The HDL-C/P ratio was calculated as HDL-cholesterol over HDL-P. Endpoint was CV death, with non-CV death as the competing event. 422 patients were included and followed-up during a median of 4.1 (0–8) years. CV death occurred in 120 (30.5%) patients. Mean HDL-Sz was higher in CV dead as compared with survivors (8.39 nm vs. 8.31 nm, p < 0.001). This change in size was due to a reduction in the percentage of small HDL-P (54.6% vs. 60% for CV-death vs. alive; p < 0.001). HDL-C/P ratio was higher in the CV-death group (51.0 vs. 48.3, p < 0.001). HDL-Sz and HDL-C/P ratio were significantly associated with CV death after multivariable regression analysis (HR 1.22 [95% CI 1.01–1.47], p = 0.041 and HR 1.04 [95% CI 1.01–1.07], p = 0.008 respectively). HDL-Sz and HDL-C/P ratio are independent predictors of CV death in chronic HF patients.Tis work was supported by Grants from Fundació La MARATÓ de TV3 (201502 and 201516 to AB-G, 201602- 30-31 to NA and JJ), Ministerio de Educación y Ciencia (SAF2014-59892 to AB-G), AdvanceCat (2014-2020 to AB-G), Ministerio de Economía y Competitividad (MINECO)—Instituto de Salud Carlos III (ISCIII) (PI17- 00232 to JJ, PI17-01362 to NA, PI15-00625 to DM, and RED2018-102799-T to JJ), and by CIBER on Cardiovascular Diseases (CIBERCV, CB16/11/00403) and CIBER for Diabetes and Associated Metabolic Diseases (CIBERDEM, CB15/00071 and CB07/08/0016) are an initiative from ISCIII, Spain with co-funding from the European Regional Development Fund (ERDF). JJ is supported by funds provided by ISCIII (Grant CPII18/00004, Miguel Servet II program)

Particle size and cholesterol content of circulating HDL correlate with cardiovascular death in chronic heart failure

Altres ajuts: Fundació la Marató de TV3: 201602-30-31; 201502Evidence regarding any association of HDL-particle (HDL-P) derangements and HDL-cholesterol content with cardiovascular (CV) death in chronic heart failure (HF) is lacking. To investigate the prognostic value of HDL-P size (HDL-Sz) and the number of cholesterol molecules per HDL-P for CV death in HF patients. Outpatient chronic HF patients were enrolled. Baseline HDL-P number, subfractions and HDL-Sz were measured using 1H-NMR spectroscopy. The HDL-C/P ratio was calculated as HDL-cholesterol over HDL-P. Endpoint was CV death, with non-CV death as the competing event. 422 patients were included and followed-up during a median of 4.1 (0-8) years. CV death occurred in 120 (30.5%) patients. Mean HDL-Sz was higher in CV dead as compared with survivors (8.39 nm vs. 8.31 nm, p < 0.001). This change in size was due to a reduction in the percentage of small HDL-P (54.6% vs. 60% for CV-death vs. alive; p < 0.001). HDL-C/P ratio was higher in the CV-death group (51.0 vs. 48.3, p < 0.001). HDL-Sz and HDL-C/P ratio were significantly associated with CV death after multivariable regression analysis (HR 1.22 [95% CI 1.01-1.47], p = 0.041 and HR 1.04 [95% CI 1.01-1.07], p = 0.008 respectively). HDL-Sz and HDL-C/P ratio are independent predictors of CV death in chronic HF patients