Dual-Band Transmitter and Receiver with Bowtie-Antenna in 0.13 μm SiGe BiCMOS for Gas Spectroscopy at 222 - 270 GHz

This paper presents a transmitter (TX) and a receiver (RX) with bowtie-antenna and silicon lens for gas spectroscopy at 222-270 GHz, which are fabricated in IHP’s 0.13 μm SiGe BiCMOS technology. The TX and RX use two integrated local oscillators for 222 – 256 GHz and 250 – 270 GHz, which are switched for dual-band operation. Due to its directivity of about 27 dBi, the single integrated bowtie-antenna with silicon lens enables an EIRP of about 25 dBm for the TX, and therefore a considerably higher EIRP for the 2-band TX compared to previously reported systems. The double sideband noise temperature of the RX is 20,000 K (18.5 dB noise figure) as measured by the Y-factor method. Absorption spectroscopy of gaseous methanol is used as a measure for the performance of the gas spectroscopy system with TX- and RX-modules

Activation of Autophagy in a Rat Model of Retinal Ischemia following High Intraocular Pressure

Acute primary open angle glaucoma is an optic neuropathy characterized by the elevation of intraocular pressure, which causes retinal ischemia and neuronal death. Rat ischemia/reperfusion enhances endocytosis of both horseradish peroxidase (HRP) or fluorescent dextran into ganglion cell layer (GCL) neurons 24 h after the insult. We investigated the activation of autophagy in GCL-neurons following ischemia/reperfusion, using acid phosphatase (AP) histochemistry and immunofluorescence against LC3 and LAMP1. Retinal I/R lead to the appearance of AP-positive granules and LAMP1-positive vesicles 12 and 24 h after the insult, and LC3 labelling at 24 h, and induced a consistent retinal neuron death. At 48 h the retina was negative for autophagic markers. In addition, Western Blot analysis revealed an increase of LC3 levels after damage: the increase in the conjugated, LC3-II isoform is suggestive of autophagic activity. Inhibition of autophagy by 3-methyladenine partially prevented death of neurons and reduces apoptotic markers, 24 h post-lesion. The number of neurons in the GCL decreased significantly following I/R (I/R 12.21±1.13 vs controls 19.23±1.12 cells/500 µm); this decrease was partially prevented by 3-methyladenine (17.08±1.42 cells/500 µm), which potently inhibits maturation of autophagosomes. Treatment also prevented the increase in glial fibrillary acid protein immunoreactivity elicited by I/R. Therefore, targeting autophagy could represent a novel and promising treatment for glaucoma and retinal ischemia

Quasi-continuous frequency tunable terahertz quantum cascade lasers with coupled cavity and integrated photonic lattice

We demonstrate quasi-continuous tuning of the emission frequency from coupled cavity terahertz frequency quantum cascade lasers. Such coupled cavity lasers comprise a lasing cavity and a tuning cavity which are optically coupled through a narrow air slit and are operated above and below the lasing threshold current, respectively. The emission frequency of these devices is determined by the Vernier resonance of longitudinal modes in the lasing and the tuning cavities, and can be tuned by applying an index perturbation in the tuning cavity. The spectral coverage of the coupled cavity devices have been increased by reducing the repetition frequency of the Vernier resonance and increasing the ratio of the free spectral ranges of the two cavities. A continuous tuning of the coupled cavity modes has been realized through an index perturbation of the lasing cavity itself by using wide electrical heating pulses at the tuning cavity and exploiting thermal conduction through the monolithic substrate. Single mode emission and discrete frequency tuning over a bandwidth of 100 GHz and a quasi-continuous frequency coverage of 7 GHz at 2.25 THz is demonstrated. An improvement in the side mode suppression and a continuous spectral coverage of 3 GHz is achieved without any degradation of output power by integrating a π-phase shifted photonic lattice in the laser cavity

Proneuropeptide Y and neuropeptide Y metabolites in healthy volunteers and patients with a pheochromocytoma or paraganglioma

Neuropeptide Y (NPY1-36) is a vasoconstrictor peptide co-secreted with catecholamines by sympathetic nerves, the adrenal medulla, and neoplasms such as pheochromocytomas and paragangliomas (PPGLs). It is produced by the intracellular cleavage of proNPY and metabolized into multiple fragments with distinct biological activities. NPY immunoassays for PPGL have a diagnostic sensitivity ranging from 33 to 100%, depending on the antibody used. We have validated a multiplex micro-UHPLC-MS/MS assay for the specific and sensitive quantification of proNPY, NPY1-39, NPY1-37, NPY1-36, NPY2-36, NPY3-36, NPY1-35, NPY3-35, and the C-flanking peptide of NPY (CPON) (collectively termed NPYs), and determined the NPYs reference intervals and concentrations in 32 PPGL patients before, during, and after surgery. Depending on the peptide measured, NPYs were above the upper reference limit (URL) in 20% to 67% of patients, whereas plasma free metanephrine and normetanephrine, the gold standard for PPGL, were above the URL in 40% and 87% of patients, respectively. Age, sex, tachycardia, and tumor localization were not correlated with NPYs. Plasma free metanephrines performed better than NPYs in the detection of PPGL, but NPYs may be a substitute for an early diagnosis of PPGL for patients that suffer from severe kidney impairment or receiving treatments that interfere with catecholamine reuptake

Expiratory flow rate, breath hold and anatomic dead space influence electronic nose ability to detect lung cancer

BACKGROUND: Electronic noses are composites of nanosensor arrays. Numerous studies showed their potential to detect lung cancer from breath samples by analysing exhaled volatile compound pattern ("breathprint"). Expiratory flow rate, breath hold and inclusion of anatomic dead space may influence the exhaled levels of some volatile compounds; however it has not been fully addressed how these factors affect electronic nose data. Therefore, the aim of the study was to investigate these effects. METHODS: 37 healthy subjects (44 +/- 14 years) and 27 patients with lung cancer (60 +/- 10 years) participated in the study. After deep inhalation through a volatile organic compound filter, subjects exhaled at two different flow rates (50 ml/sec and 75 ml/sec) into Teflon-coated bags. The effect of breath hold was analysed after 10 seconds of deep inhalation. We also studied the effect of anatomic dead space by excluding this fraction and comparing alveolar air to mixed (alveolar + anatomic dead space) air samples. Exhaled air samples were processed with Cyranose 320 electronic nose. RESULTS: Expiratory flow rate, breath hold and the inclusion of anatomic dead space significantly altered "breathprints" in healthy individuals (p 0.05). These factors also influenced the discrimination ability of the electronic nose to detect lung cancer significantly. CONCLUSIONS: We have shown that expiratory flow, breath hold and dead space influence exhaled volatile compound pattern assessed with electronic nose. These findings suggest critical methodological recommendations to standardise sample collections for electronic nose measurements