Modelling end-pumped solid state lasers

The operation dynamics of end-pumped solid-state lasers are investigated by means of a spatially resolved numerical rate-equation model and a time-dependent analytical thermal model. The rate-equation model allows the optimization of parameters such as the output coupler transmission and gain medium length, with the aim of improving the laser output performance. The time-dependent analytical thermal model is able to predict the temperature and the corresponding induced thermal stresses on the pump face of quasi-continuous wave (qcw) end-pumped laser rods. Both models are found to be in very good agreement with experimental results

Microglial cell dysregulation in brain aging and neurodegeneration

Aging is the main risk factor for neurodegenerative diseases. In aging, microglia undergo phenotypic changes compatible with their activation. Glial activation can lead to neuroinflammation, which is increasingly accepted as part of the pathogenesis of neurodegenerative diseases, including Alzheimer’s disease (AD). We hypothesize that in aging, aberrant microglia activation leads to a deleterious environment and neurodegeneration. In aged mice, microglia exhibit an increased expression of cytokines and an exacerbated inflammatory response to pathological changes. Whereas LPS increases nitric oxide secretion in microglia from young mice, induction of reactive oxygen species (ROS) predominates in older mice. Furthermore, there is accumulation of DNA oxidative damage in mitochondria of microglia during aging, and also an increased intracellular ROS production. Increased ROS activates the redox-sensitive nuclear factor kappa B, which promotes more neuroinflammation, and can be translated in functional deficits, such as cognitive impairment. Mitochondria-derived ROS and cathepsin B, are also necessary for the microglial cell production of interleukin-1β, a key inflammatory cytokine. Interestingly, whereas the regulatory cytokine TGFβ1 is also increased in the aged brain, neuroinflammation persists. Assessing this apparent contradiction, we have reported that TGFβ1 induction and activation of Smad3 signaling after inflammatory stimulation are reduced in adult mice. Other protective functions, such as phagocytosis, although observed in aged animals, become not inducible by inflammatory stimuli and TGFβ1. Here, we discuss data suggesting that mitochondrial and endolysosomal dysfunction could at least partially mediate age-associated microglial cell changes, and, together with the impairment of the TGFβ1-Smad3 pathway, could result in a reduction of protective activation and a facilitation of cytotoxic activation of microglia, resulting in the promotion of neurodegeneration

Narrow-Linewidth Distributed Feedback Channel Waveguide Laser in Al2_2O3_3:Er3+^{3+}

We report on the fabrication and characterization of a distributed feedback channel waveguide laser in erbium-doped aluminium oxide on a standard thermally oxidized silicon substrate. Holographically-written surface-relief Bragg gratings have been integrated with the aluminium oxide waveguides via reactive ion etching of a silicon dioxide overlay film. The laser operates at a wavelength of 1545.2 nm and exhibits a threshold of 2.2 mW absorbed pump power, while it produces a maximum output power of 3 mW. The emission is TE polarized and has a Lorentzian linewidth of 1.70±0.58 kHz, which corresponds to a Q-factor of 1.14×E11

High-Q distributed-Bragg-grating laser cavities

Applying Bragg gratings in Al2O3 channel waveguides, we demonstrate distributed Bragg reflectors with Q-factors of 1.02x10e6. An integrated Al2O3:Yb3+ waveguide laser with 67% slope efficiency and 47 mW output power is achieved with such cavities

Physical activity heterogenously modulates NG2-glia population behavior, and is necessary for cognitive enhancement

NG2-glia is a macroglial population, which constitutes about 5-10% of the total cell population in the mammalian brain. These cells have “stem cell-like” features; for instance, they can proliferate and self-renew and they mostly differentiate into oligodendrocytes, a cell type are of great importance as they myelinate axons in the central nervous system, a process essential for the proper function of vertebrates’ nervous system. Although most myelination happens after birth and completed at a young age, it has been shown that it can also occur during adulthood in mammals. Adult myelination can be modulated by experience, but the exact mechanism of this phenomenon remains unclear. Hence, it is thought that neuronal activity could stop the proliferation and promote the differentiation of NG2-glia, and in turn, newly generated oligodendrocytes could provide the new myelin. However, it is still unclear how neuronal activity could lead to changes in NG2-glia behavior in the adult mouse. In this doctoral thesis, I have used a voluntary physical activity (VPA) mouse model to study the effects of experience on NG2-glia, although other mechanism cannot be discarded. Indeed, our results showed an increase in the proliferation and differentiation of NG2-glia in the cerebral cortical grey matter but not in the corresponding white matter after VPA. We also observed that NG2-glia tend to differentiate with two different modalities, and one of them is preferred during VPA. Furthermore, I performed mass spectrometry of sorted NG2-glia to profile them after VPA, and found that the remaining, non-differentiated NG2-glia show less myelin-related proteins. Interestingly, the results of the proteome analysis correlate with the increase in the number of the GPR17+ subset of NG2-glia, which is characterized by its slow differentiation rate, and I observed that this population remains mostly unaffected by VPA. Finally, for the first time, I found that newly generated oligodendrocytes integrate into the circuitry of the cortex and this myelin remodeling contributes in cognitive enhancement induced by exercise

Ultra-high, broadband gain in a lattice-engineered, Yb-doped double tungstate channel waveguide

150 dB/cm gain over 55 nm wavelength range between 977-1032 nm is obtained in a 47.5% Yb-doped potassium double tungstate waveguide amplifier. The dependence of luminescence lifetime and gain on Yb concentration is investigated

Single-Frequency, Narrow-Linewidth Distributed Feedback Waveguide Laser in Al2O3:Er3+ on Silicon

A distributed feedback channel waveguide laser in erbium-doped aluminum oxide on a silicon substrate is reported. The optically pumped laser has a threshold pump power of 15 mW and emits 3 mW in single-frequency operation at 1545.2 nm wavelength with a slope efficiency of 6.2% and linewidth of 15 kHz

Age-dependent changes on fractalkine forms and their contribution to neurodegenerative diseases

The chemokine fractalkine (FKN, CX3CL1), a member of the CX3C subfamily, contributes to neuron–glia interaction and the regulation of microglial cell activation. Fractalkine is expressed by neurons as a membrane-bound protein (mCX3CL1) that can be cleaved by extracellular proteases generating several sCX3CL1 forms. sCX3CL1, containing the chemokine domain, and mCX3CL1 have high affinity by their unique receptor (CX3CR1) which, physiologically, is only found in microglia, a resident immune cell of the CNS. The activation of CX3CR1contributes to survival and maturation of the neural network during development, glutamatergic synaptic transmission, synaptic plasticity, cognition, neuropathic pain, and inflammatory regulation in the adult brain. Indeed, the various CX3CL1 forms appear in some cases to serve an anti-inflammatory role of microglia, whereas in others, they have a pro-inflammatory role, aggravating neurological disorders. In the last decade, evidence points to the fact that sCX3CL1 and mCX3CL1 exhibit selective and differential effects on their targets. Thus, the balance in their level and activity will impact on neuron–microglia interaction. This review is focused on the description of factors determining the emergence of distinct fractalkine forms, their age-dependent changes, and how they contribute to neuroinflammation and neurodegenerative diseases. Changes in the balance among various fractalkine forms may be one of the mechanisms on which converge aging, chronic CNS inflammation, and neurodegeneration