Low frequency noise conversion in fets under nonlinear operation

Based upon the active line concept, the conversion mechanisms of microscopic low frequency noise (e.g. generation-recombination noise) located in the channel of a Field Effect Transistor (FET) which is driven by a large RF signal is demonstrated. The first consequence is that the based band (low frequency) input gate noise voltage spectral density is dependent on the magnitude of the input RF power applied to the FET. Moreover, the microscopic generation-recombination noise sources located in the channel are responsible of up-converted input gate noise voltage spectral density around the RF frequency

Nonlinear noise modeling of a PHEMT device through residual phase noise and low frequency noise measurements

International audienceThe phase noise generated by a FET device is investigated using transmission and reflection residual phase noise measurements. This approach helps in locating, in the intrinsic device, the low frequency noise sources which are responsible for these phase fluctuations. On the basis of these experiments, a new nonlinear noise model of the FET is proposed. This model is able to describe a phenomenon that has been observed, but never modeled in the past : the dependence of the baseband noise on the microwave input power

Impact of gamma irradiation on the RF phase noise capability of UHV/CVD SiGe HBTs

This work investigates the effects of gamma irradiation on the residual phase noise of SiGe HBTs. The excellent phase noise capabioity of SiGe HBT is retained after 1Mrad(si) irradiation. The observed radiation hardness is attributed to the minor changes in the low frequency noise and device nonlinearities after irradiations, as well as the nonlinearity cancellation mechanism. The radiation-induced defects do not significantly add to the low frequency noise in these SiGe HBTs, even though they produce a large space-charge-region recombination component in the base current. The inherent excellent linearity of these SiGe HBTs makes the up-conversion from device low frequency noise to phase noise inefficient, and helps to retain the low pahse noise after irradiations

Barhl2 limits growth of the diencephalic primordium through Caspase3 inhibition of β-catenin activation

Little is known about the respective contributions of cell proliferation and cell death to the control of vertebrate forebrain growth. The homeodomain protein barhl2 is expressed in the diencephalons of Xenopus, zebrafish, and mouse embryos, and we previously showed that Barhl2 overexpression in Xenopus neuroepithelial cells induces Caspase3-dependent apoptosis. Here, barhl2 is shown to act as a brake on diencephalic proliferation through an unconventional function of Caspase3. Depletion of Barhl2 or Caspase3 causes an increase in diencephalic cell number, a disruption of the neuroepithelium architecture, and an increase in Wnt activity. Surprisingly, these changes are not caused by decreased apoptosis but instead, are because of an increase in the amount and activation of β-catenin, which stimulates excessive neuroepithelial cell proliferation and induces defects in β-catenin intracellular localization and an up-regulation of axin2 and cyclinD1, two downstream targets of β-catenin/T-cell factor/lymphoïd enhancer factor signaling. Using two different sets of complementation experiments, we showed that, in the developing diencephalon, Caspase3 acts downstream of Barhl2 in limiting neuroepithelial cell proliferation by inhibiting β-catenin activation. Our data argue that Bar homeodomain proteins share a conserved function as cell type-specific regulators of Caspase3 activities

Development and regeneration of the vertebrate brain

The vertebrate brain is hierarchically assembled about orthogonal axes using organizing centers that control cascades of signaling events. The reiterative generation of these centers at defined times, and in precise spatial locations, leads to the conversion of a contiguous and homogenous epithelial sheet into the most complex biological tissue in the animal kingdom. The critical events orchestrating the construction of a "typical" vertebrate brain are described. Attention is focused on specification of major brain regions common across the vertebrate phylogeny, rather than on the differentiation of constituent cell types and specific cytoarchitectures. By uncloaking the complex spatial interactions that unfold temporally during the build of the vertebrate brain, it becomes clear why regeneration of this tissue following injury is such a challenging task. And yet, while mammalian brains fail to regenerate, the brains of non-mammalian vertebrates, such as teleosts, reptiles and amphibians, can successfully reconstitute brain tissue following traumatic injury. Understanding the molecular and cellular bases of this remarkable regenerative capacity is revealing the importance of developmental programs, as well as exposing unexpected roles for extraneous processes such as inflammation. Recent discoveries are now fuelling hope for future therapeutic approaches that will ameliorate the debilitating consequences of brain injury in humans