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BackgroundAlthough the relationship between allergic inflammation and lung carcinogenesis is not clearly defined, several reports suggest an increased incidence of lung cancer in patients with asthma. We aimed at determining the functional impact of allergic inflammation on chemical carcinogenesis in the lungs of mice.MethodsBalb/c mice received single-dose urethane (1 g/kg at day 0) and two-stage ovalbumin during tumor initiation (sensitization: days -14 and 0; challenge: daily at days 6-12), tumor progression (sensitization: days 70 and 84; challenge: daily at days 90-96), or chronically (sensitization: days -14 and 0; challenge: daily at days 6-12 and thrice weekly thereafter). In addition, interleukin (IL)-5 deficient and wild-type C57BL/6 mice received ten weekly urethane injections. All mice were sacrificed after four months. Primary end-points were number, size, and histology of lung tumors. Secondary end-points were inflammatory cells and mediators in the airspace compartment.ResultsOvalbumin provoked acute allergic inflammation and chronic remodeling of murine airways, evident by airspace eosinophilia, IL-5 up-regulation, and airspace enlargement. Urethane resulted in formation of atypical alveolar hyperplasias, adenomas, and adenocarcinomas in mouse lungs. Ovalbumin-induced allergic inflammation during tumor initiation, progression, or continuously did not impact the number, size, or histologic distribution of urethane-induced pulmonary neoplastic lesions. In addition, genetic deficiency in IL-5 had no effect on urethane-induced lung tumorigenesis.ConclusionsAllergic inflammation does not impact chemical-induced carcinogenesis of the airways. These findings suggest that not all types of airway inflammation influence lung carcinogenesis and cast doubt on the idea of a mechanistic link between asthma and lung cancer.

A general analysis on stochastic timing errors (clock or timing jitter) is presented for Digital to Analog Converters (DAC). The obtained results describe the effects of (non)correlated errors for given signal properties, and reveal the nature of the tradeoff between oversampling ratio, resolution and noise shaping in the context of noise-shaped DACs and Continuous-Time (CT) Sigma Delta (EA) ADCs. The importance of timing jitter for wideband DAC performance is exemplified with theory and simulations.

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This paper presents a parallel sampling technique for analog-to-digital converters (ADCs) to convert multi-carrier signals efficiently by exploiting the statistical properties of these signals. With this technique, the input signal power of an ADC can be boosted without getting excessive clipping distortion and the ADC can have a higher resolution over the critical small amplitude region. Hence the overall signal to noise and clipping distortion ratio is improved. This technique allows reducing power dissipation and area in comparison to conventional solutions for converting multicarrier signals. As an example, an 11b switched-capacitor pipeline ADC with the parallel sampling technique applied to its first stage is implemented in CMOS 65 nm technology. It achieves a full-scale input signal range of 2 V differentially with a 1.2 V supply voltage. Simulations show an improvement of more than 5 dB in signal-tonoise-and-clipping-distortion ratio (SNCDR) and around 8 dB in dynamic range (DR) compared to a conventional 11b ADC for converting multi-carrier signals and achieve a comparable SNCDR and noise power ratio (NPR) as a conventional 12b pipeline for converting multi-carrier signals with less than half the power and area.Index Terms-Analog-to-digital converters, dynamic range, multi-carrier signals, noise power ratio, parallel sampling technique, switched-capacitor pipeline ADC.