206 research outputs found
UV-A Radiation: Safe Human Exposure and Antibacterial Activity
No full text: UV radiation is used for sterilization but has adverse health effects in humans. UV-A radiation has lower antimicrobial effect than UV-B and UV-C but constitutes a lower health risk, opening up the possibility to sanitize environments with human presence in controlled exposure conditions. We investigated this possibility by identifying safe exposure conditions to a UV-A lamp along with efficient sanitization of the environment. The human exposure limits were calculated following the guidelines provided by the International Commission on Non-Ionizing Radiation Protection and the International Commission on Illumination. Antibacterial activity was evaluated on Escherichia coli, Pseudomonas aeruginosa and Staphylococcus aureus. The maximum human exposure duration has been identified at different irradiation distance and angle, increasing with the increase of both parameters. Bactericidal activity was observed in all microorganisms and was higher with higher exposure time and at lower distance from the source. Noteworthily, in equal conditions of radiant exposure, the exposure time impacts on the bactericidal activity more than the distance from the source. The modulation of factors such as distance from the source, exposure time and irradiation angle can enable effective antibacterial activity and human safety. Prolonged direct irradiation of the surfaces associated with indirect human exposure represents the condition of greater efficacy and safety
lleo meconial
No full textThe term Meconium Ileus refers to three different conditions of similar pathologic anatomy and clinicalfeatures. but very different prognosis and ·treatment. The author describes: 1) Classic Meconium Ileus and its complications being an affection of high inmediate, mediate and latemortality. 2) The Meconium Plug Síndrome of easy resolution and good prognosis when ever correct diagnosis is established. 3) Meconium obstruction in the absence of mucoviscidosisa rare afection associa ted with intestinal absortive anomalies and whose prognosis is better than of Classic Meconium Ileus.El término ileo meconial comprende tres entidades nosológicas con similitud anatomoclínica pero que difieren en su pronóstico y tratamiento.Se describen: el I. M. Clásico y sus complicaciones con su elevado porcentaje de mortalidad inmediata, mediata y tardía. El síndrome del tapón meconial defácil resolución y buen pronóstico una vez diagnosticado. Por último, el I. M. no asociado a mucoviscidosis, afección rara relacionada con trastornos disabsortivosy cuyo pronóstico es más favorable que el I M. Clásico
Clinical course of Alzheimer’s disease
No full text• Alzheimer’s disease is an age-related neurodegenerative disorder, with onset usually in late life, characterized by cognitive impairment, a variety of behavioural symptoms, and restrictions in the activities of daily living• The initial symptom is episodic memory loss, in particular in delayed recall of visual and/or verbal material. Immediate and remote memory is usually preserved in early stages...</p
Complex Neuroimaging Changes in Metabolite, Cortical Structures and Regional Vulnerabilities in the Alzheimer Disease Continuum
No full textLa enfermedad de Alzheimer es la principal causa de demencia. Patológicamente, está caracterizada
por tau hiperfosforilada intracelular y el depósito de placas de amiloide extracelular. Estos procesos
fisiopatológicos empiezan décadas antes de que aparezca el deterioro cognitivo, y conllevan atrofia
cerebral y neurodegeneracion. La imagen por resonancia magnética (RM) nos permite caracterizar “invivo”
los cambios corticales en las fases preclínicas de la enfermedad. Esta tesis incluye trabajos donde
se estudian los cambios macroestructurales, microestrucutrales y de metabolitos corticales a lo largo del
continuo de la EA. Este trabajo destaca la complejidad de estos cambios y su trayectoria no lineal, y
analiza la vulnerabilidad regional que subyace a la propagación de tau en las fases tempranas de la
enfermedad. En concreto, en el primer trabajo de esta tesis, se modeló matemáticamente la trayectoria
de cambios de grosor cortical y difusividad cortical en la EA autosómica dominante. Demostramos que
existe los cambios corticales siguen una trayectoria bifásica, donde en el inicio y relacionado con el
acúmulo de amiloide, aparece un incremento del grosor cortical y un descenso de la difusividad
cortical, que siguen a cambios hacia atrofia e incrementos de difusividad una vez tau adquiere valores
patológicos (15 años antes de que empiecen los síntomas clínicos). En el segundo trabajo de esta tesis
se caracterizó las alteraciones de metabolitos en el continuo de la EA en una muestra de adultos con
Síndrome de Down usando resonancia magnética por espectroscopia (RMS). Este estudio demuestra el
potencial de la RMS para detectar alteraciones relacionadas con la neurodegeneracion en la EA. En el
tercer trabajo de esta tesis se investigó el potencial de la difusividad cortical como marcador de
neurodegeneracion, y su relación con el acúmulo patológico de tau en las fases preclínicas de la EA. En
el cuarto trabajo de esta tesis se estudió el perfil genético de la vulnerabilidad regional asociada al
patrón de propagación de tau. Para este trabajo se desarrollaron herramientas basadas en teoría de
grafos para caracterizar la propagación de tau, integrando información de alta resolución sobre
expresión génica. Esta tesis supone potenciales implicaciones. En primer lugar, consolida la presencia
de un modelo bifasico de cambios corticales que proporciona una explicacion a resultados
aparentemente adversos en la literatura, y propone el potencial de la RM para capturar alteraciones
estructurales en las etapas tempranas de la enfermedad. En segundo lugar, demuestra el potencial de la
RMS como marcador no invasico para medir la neurodegeneracion e inflamacion en la poblacion con
Sindrome de Down. En tercer lugar, propone que la difusividad cortical es un potencial marcador de
neurodegeneracion mas sensible que el grosor cortical, con potencial para ser usado en ensayos
clinicos. En ultimo lugar, propone un marco analitico para estudiar las vulnerabilidades regionales
asociadas a la propagacion de tau, cuyos resultados pueden suponer una guia de investigacion a nuevas
dianas farmacologicas. En conclusion, esta tesis destaca la complejidad de los cambios corticales en
etapas preclinicas de la EA y su vulnerabilidad regional.Alzheimer disease (AD) is the most important cause of dementia. Its histopathological hallmarks are
intracellular hyperphosphorylated tau and extracellular amyloid plaques, which start to accumulate
decades before the onset of clinical symptoms and eventually lead to neurodegeneration and brain
atrophy. Magnetic resonance imaging (MRI) provides a window to characterize in vivo the cortical
changes in the preclinical and clinical phases of the disease. This thesis studied the cortical
macrostructural, microstructural and metabolite changes along the AD continuum. It highlights the
complex and non-linear alterations in the preclinical phase and analyzes the characteristic regional
vulnerability underlying the spread of tau in early stages of the disease. Specifically, the first work of
the thesis mathematically modeled the trajectory of cortical thickness and cortical mean diffusivity in
autosomal dominant Alzheimer disease. This work demonstrated a biphasic trajectory of cortical
alterations, in which the initial increases of amyloid were associated with increased cortical thickness
and decreased cortical diffusivity, but were followed by cortical thinning and increased cortical
diffusivity once tau becomes abnormal (15 years prior to symptom onset). The second work of this
thesis characterized the alterations of metabolites along the AD continuum in a cohort of Down
Syndrome using magnetic resonance spectroscopy (MRS). This work showed the potential of MRS to
detect AD-related inflammation and neurodegeneration. The third work of this thesis investigated the
potential of cortical diffusivity as a marker of neurodegeneration and its relationship with the
accumulation of tau in preclinical AD. This work showed cortical diffusivity decreases were associated
with the accumulation of tau in inferior temporal regions and predicted clinical deterioration. The
fourth work of this thesis studied the genetic regional vulnerability associated to the stereotypical
pattern of tau accumulation. This work developed a novel graph-theory-based framework to
characterize the spread of tau integrating a high-resolution data of gene expression. This thesis has
several important potential implications. First, it consolidates the biphasic trajectory of cortical
alterations that reconciles previous conflicting results in the literature, greatly expand the potential of
MRI to track changes in preclinical AD and provides a rationale to understand the (otherwise)
paradoxical findings of increased atrophy in the active arm of anti-amyloid trials. Second, this thesis
showed MRS could be a good noninvasive disease-stage biomarker in Down syndrome to track
neurodegeneration and neuroinflammation. Third, it shows cortical mean diffusivity could be a more
sensitive marker of neurodegeneration than cortical thickness that could be implemented in clinical
trials. Finally, it provides a new framework to analyze the regional vulnerability underlying the spread
of tau which could lead to the identification of new drug targets. In conclusion, this thesis highlights
the complexity of the cortical changes preclinical AD and their regional vulnerability, but also
demonstrates the potential of MRI to track these changes when using a multimodal approach, nonlinear
models and new analytical frameworks.Universitat Autònoma de Barcelona. Programa de Doctorat en Neurocièncie
Non-fibrillar oligomeric amyloid-β within synapses: Data set from publication Pickett et al 2016 J Alz Dis
No full textAlzheimer’s disease (AD) is characterized by memory loss, insidious cognitive decline, profound neurodegeneration and the extracellular accumulation of amyloid-beta (Ab) peptide in senile plaques and intracellular accumulation of tau in neurofibrillary tangles. Loss and dysfunction of synapses are believed to underlie the devastating cognitive decline in AD. A large amount of evidence suggests that oligomeric forms of Ab associated with senile plaques are toxic to synapses, but the precise sub-synaptic localization of Ab and which forms are synaptotoxic remain unknown. Here, we characterize the sub-synaptic localization of Ab oligomers using three high-resolution imaging techniques, stochastic optical reconstruction microscopy, immunogold electron microscopy and Förster resonance energy transfer in a plaque-bearing mouse model of Alzheimer’s disease. With all three techniques, we observe oligomeric Ab inside synaptic terminals. Further, we tested a panel of Ab antibodies using the relatively high-throughput array tomography technique to determine which forms are present in synapses. Our results show that different oligomeric Ab species are present in synapses and highlight the potential of array tomography for rapid testing of aggregation state specific Ab antibodies in brain tissue.Pickett, Eleanor K.; Koffie, Robert M.; Wegmann, Susanne; Henstridge, Christopher M.; Herrmann, Abigail G.; Colom-Cadena, Marti; Lleo, Alberto; Kay, Kevin R.; Vaught, Melissa; Soberman, Roy; Walsh, Dominic M.; Hyman, Bradley T.; Spires-Jones, Tara L. (2016). Non-fibrillar oligomeric amyloid-β within synapses: Data set from publication Pickett et al 2016 J Alz Dis, [dataset]. University of Edinburgh. School of Biomedical Sciences. http://dx.doi.org/10.7488/ds/1415
&#947;-Secretase Substrates and their Implications for Drug Development in Alzheimer's Disease
No full textCOVID-19 Digestive System Involvement and Clinical Outcomes in a Large Academic Hospital in Milan, Italy
No full textSince February 2020, the COVID-19 pandemic has spread to Italy affecting more than 100,000 people. Several studies have reported a high prevalence of gastrointestinal (GI) symptoms, and investigated their potential association with clinical outcomes.1 The timing, clinical significance, and possible impact on viral spread of GI symptoms presentation have not been fully elucidated. Elevation of liver function tests and other laboratory values has also been reported; however, their prognostic significance has not been clearly established.2
Non-fibrillar oligomeric amyloid-β within synapses: Data set from publication Pickett et al 2016 J Alz Dis
No full textAlzheimer’s disease (AD) is characterized by memory loss, insidious cognitive decline, profound neurodegeneration and the extracellular accumulation of amyloid-beta (Ab) peptide in senile plaques and intracellular accumulation of tau in neurofibrillary tangles. Loss and dysfunction of synapses are believed to underlie the devastating cognitive decline in AD. A large amount of evidence suggests that oligomeric forms of Ab associated with senile plaques are toxic to synapses, but the precise sub-synaptic localization of Ab and which forms are synaptotoxic remain unknown. Here, we characterize the sub-synaptic localization of Ab oligomers using three high-resolution imaging techniques, stochastic optical reconstruction microscopy, immunogold electron microscopy and Förster resonance energy transfer in a plaque-bearing mouse model of Alzheimer’s disease. With all three techniques, we observe oligomeric Ab inside synaptic terminals. Further, we tested a panel of Ab antibodies using the relatively high-throughput array tomography technique to determine which forms are present in synapses. Our results show that different oligomeric Ab species are present in synapses and highlight the potential of array tomography for rapid testing of aggregation state specific Ab antibodies in brain tissue
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