A 400-to-900 MHz Receiver with Dual-domain Harmonic Rejection Exploiting Adaptive Interference Cancellation

Wideband direct-conversion harmonic-rejection (HR) receivers for software-defined radio aim to remove or relax the pre-mixer RF filters, which are inflexible, bulky and costly [1,2]. HR schemes derived from [3] are often used, but amplitude and phase mismatches limit HR to between 30 and 40dB [1,2]. A quick calculation shows that much more rejection is wanted: in order to bring harmonic responses down to the noise floor (e.g. −100dBm in 10MHz for 4dB NF), and cope with interferers between −40 and 0dBm, an HR of 60 to 100dB is needed. Also in terrestrial TV receivers and in applications like DVB-H with co-existence requirements with GSM/WLAN transmitters in a small telephone, high HR is needed

Digitally-Enhanced Software-Defined Radio Receiver Robust to Out-of-Band Interference

A software-defined radio (SDR) receiver with improved robustness to out-of-band interference (OBI) is presented. Two main challenges are identified for an OBI-robust SDR receiver: out-of-band nonlinearity and harmonic mixing. Voltage gain at RF is avoided, and instead realized at baseband in combination with low-pass filtering to mitigate blockers and improve out-of-band IIP3. Two alternative “iterative” harmonic-rejection (HR) techniques are presented to achieve high HR robust to mismatch: a) an analog two-stage polyphase HR concept, which enhances the HR to more than 60 dB; b) a digital adaptive interference cancelling (AIC) technique, which can suppress one dominating harmonic by at least 80 dB. An accurate multiphase clock generator is presented for a mismatch-robust HR. A proof-of-concept receiver is implemented in 65 nm CMOS. Measurements show 34 dB gain, 4 dB NF, and 3.5 dBm in-band IIP3 while the out-of-band IIP3 is + 16 dBm without fine tuning. The measured RF bandwidth is up to 6 GHz and the 8-phase LO works up to 0.9 GHz (master clock up to 7.2 GHz). At 0.8 GHz LO, the analog two-stage polyphase HR achieves a second to sixth order HR > dB over 40 chips, while the digital AIC technique achieves HR > 80 dB for the dominating harmonic. The total power consumption is 50 mA from a 1.2 V supply

Proteus II: design and evaluation of an integrated power-efficient underwater sensor node

We describe the design and evaluation of an integrated low-cost underwater sensor node designed for reconfigurability, allowing continuous operation on a relatively small rechargeable battery for one month. The node uses a host CPU for the network protocols and processing sensor data and a separate CPU performs signal processing for the ultrasonic acoustic software-defined Modulator/Demodulator (MODEM). A Frequency Shift Keying- (FSK-) based modulation scheme with configurable symbol rates, Hamming error correction, and Time-of-Arrival (ToA) estimation for underwater positioning is implemented. The onboard sensors, an accelerometer and a temperature sensor, can be used to measure basic environmental parameters; additional internal and external sensors are supported through industry-standard interfaces (I2C, SPI, and RS232) and an Analog to Digital Converter (ADC) for analog peripherals. A 433 MHz radio can be used when the node is deployed at the surface. Tests were performed to validate the low-power operation. Moreover the acoustic communication range and performance and ToA capabilities were evaluated. Results show that the node achieves the one-month lifetime, is able to perform communication in highly reflective environments, and performs ToA estimation with an accuracy of about 1-2 meters

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

A T-DAB Field Trial Using a Low-Mast Infrastructure

A novel low-mast low-power Terrestrial Digital Audio Broadcasting (T-DAB) single frequency network topology is described and evaluated in this paper. For this purpose, a pilot network (band III and L-band) was constructed in Amsterdam, the Netherlands. The performance of the band III pilot network (channel 12B) is compared with the existing traditional high-power high-mast T-DAB network (channel 12C) of the public service broadcaster. An important goal is to investigate whether the pilot network can co-exist with an existing traditional T-DAB network. The field trial shows that a gap filler can effectively neutralize the adjacent channel interference of the pilot network on the existing T-DAB network. Moreover, the L-band pilot network is compared with both band III networks by assessing the indoor coverage of every network. For estimation of the indoor coverage, 34 objects were investigated. Both the indoor penetration loss for band III and L-band was determined for each object. Indoor coverage in a region is reached if 95% of the buildings or more have indoor coverage. Using this definition, the loss for band III is 21.6 dB and for L-band 24.6 dB. As a result we consider the indoor penetration loss values reported in literature as too optimistic. Also other parameters of the pilot network were measured, such as the frequency re-use distance

Liver dysfunction and phosphatidylinositol-3-kinase signalling in early sepsis: experimental studies in rodent models of peritonitis

BACKGROUND: Hepatic dysfunction and jaundice are traditionally viewed as late features of sepsis and portend poor outcomes. We hypothesized that changes in liver function occur early in the onset of sepsis, yet pass undetected by standard laboratory tests. METHODS AND FINDINGS: In a long-term rat model of faecal peritonitis, biotransformation and hepatobiliary transport were impaired, depending on subsequent disease severity, as early as 6 h after peritoneal contamination. Phosphatidylinositol-3-kinase (PI3K) signalling was simultaneously induced at this time point. At 15 h there was hepatocellular accumulation of bilirubin, bile acids, and xenobiotics, with disturbed bile acid conjugation and drug metabolism. Cholestasis was preceded by disruption of the bile acid and organic anion transport machinery at the canalicular pole. Inhibitors of PI3K partially prevented cytokine-induced loss of villi in cultured HepG2 cells. Notably, mice lacking the PI3Kγ gene were protected against cholestasis and impaired bile acid conjugation. This was partially confirmed by an increase in plasma bile acids (e.g., chenodeoxycholic acid [CDCA] and taurodeoxycholic acid [TDCA]) observed in 48 patients on the day severe sepsis was diagnosed; unlike bilirubin (area under the receiver-operating curve: 0.59), these bile acids predicted 28-d mortality with high sensitivity and specificity (area under the receiver-operating curve: CDCA: 0.77; TDCA: 0.72; CDCA+TDCA: 0.87). CONCLUSIONS: Liver dysfunction is an early and commonplace event in the rat model of sepsis studied here; PI3K signalling seems to play a crucial role. All aspects of hepatic biotransformation are affected, with severity relating to subsequent prognosis. Detected changes significantly precede conventional markers and are reflected by early alterations in plasma bile acids. These observations carry important implications for the diagnosis of liver dysfunction and pharmacotherapy in the critically ill. Further clinical work is necessary to extend these concepts into clinical practice. Please see later in the article for the Editors' Summary

Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356

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