Design and implementation of a low-power hybrid capacitive MEMS oscillator

This paper reports on the design and implementation of a low power MEMS oscillator based on capacitively transduced silicon micromachined resonators. The analysis shows how design parameters of MEMS resonator impact on the power requirement of the oscillator, particularly with a view towards informing the impact of device and interface parasitics. The analysis is based on resonators fabricated in a 2-μm gap SOI-MEMS foundry process. The sustaining circuit, which is based on a Pierce topology, is fabricated in a standard 0.35 μm process. An automatic gain control (AGC) is adopted to suppress the mechanical non-linearity so as to improve oscillator frequency stability. The 110-kHz MEMS and CMOS dies are assembled within a standard ceramic package and electrically integrated through wire bonds. The oscillator core consumes 400 nA (900 nA with parasitic readout loading) at 1.2-V dc supply while demonstrating a frequency stability of less than 0.5 ppm. The work provides a thorough analysis and design guidelines for both MEMS and CMOS circuit design with a view towards minimizing overall power consumption. The implications of the results reported in this paper are towards enabling a new class of low power resonant MEMS sensors that utilize the oscillator as a front-end building block

A 24 GHz Sub-Harmonically Pumped Resistive Mixer in GaN HEMT Technology

—This paper presents the design and the characterization of a 24 GHz sub-harmonically pumped resistive mixer (SHM) in an advanced gallium nitride (GaN) high electron mobility transistor (HEMT) technology. The mixer is desired for building up a high-performance phaselocked W-band signal source, and is designed in a singlebalanced configuration, where the balanced LO input is generated by an on-chip first order lattice balun. In measurement, a conversion loss around 12 dB is achieved at the RF bandwidth of 22-28 GHz and the IF bandwidth of 3-6 GHz with a LO power of 10 dBm. The mixer exhibits an RF input P1dB of 13 dBm, and the measured LO to IF isolation achieves 40 dB at the desired LO of 10 GHz. To the best of the author’s knowledge, this is the first sub-harmonically pumped mixer in GaN HEMT technology

Adenosine receptor signaling: a key to opening the blood–brain door

International audienceAbstractThe aim of this review is to outline evidence that adenosine receptor (AR) activation can modulate blood–brain barrier (BBB) permeability and the implications for disease states and drug delivery. Barriers of the central nervous system (CNS) constitute a protective and regulatory interface between the CNS and the rest of the organism. Such barriers allow for the maintenance of the homeostasis of the CNS milieu. Among them, the BBB is a highly efficient permeability barrier that separates the brain micro-environment from the circulating blood. It is made up of tight junction-connected endothelial cells with specialized transporters to selectively control the passage of nutrients required for neural homeostasis and function, while preventing the entry of neurotoxic factors. The identification of cellular and molecular mechanisms involved in the development and function of CNS barriers is required for a better understanding of CNS homeostasis in both physiological and pathological settings. It has long been recognized that the endogenous purine nucleoside adenosine is a potent modulator of a large number of neurological functions. More recently, experimental studies conducted with human/mouse brain primary endothelial cells as well as with mouse models, indicate that adenosine markedly regulates BBB permeability. Extracellular adenosine, which is efficiently generated through the catabolism of ATP via the CD39/CD73 ecto-nucleotidase axis, promotes BBB permeability by signaling through A1 and A2A ARs expressed on BBB cells. In line with this hypothesis, induction of AR signaling by selective agonists efficiently augments BBB permeability in a transient manner and promotes the entry of macromolecules into the CNS. Conversely, antagonism of AR signaling blocks the entry of inflammatory cells and soluble factors into the brain. Thus, AR modulation of the BBB appears as a system susceptible to tighten as well as to permeabilize the BBB. Collectively, these findings point to AR manipulation as a pertinent avenue of research for novel strategies aiming at efficiently delivering therapeutic drugs/cells into the CNS, or at restricting the entry of inflammatory immune cells into the brain in some diseases such as multiple sclerosis