Quantum simulation of the spin-boson model with a microwave circuit

We consider superconducting circuits for the purpose of simulating the spin-boson model. The spin-boson model consists of a single two-level system coupled to bosonic modes. In most cases, the model is considered in a limit where the bosonic modes are sufficiently dense to form a continuous spectral bath. A very well known case is the ohmic bath, where the density of states grows linearly with the frequency. In the limit of weak coupling or large temperature, this problem can be solved numerically. If the coupling is strong, the bosonic modes can become sufficiently excited to make a classical simulation impossible. Here, we discuss how a quantum simulation of this problem can be performed by coupling a superconducting qubit to a set of microwave resonators. We demonstrate a possible implementation of a continuous spectral bath with individual bath resonators coupling strongly to the qubit. Applying a microwave drive scheme potentially allows us to access the strong-coupling regime of the spin-boson model. We discuss how the resulting spin relaxation dynamics with different initialization conditions can be probed by standard qubit-readout techniques from circuit quantum electrodynamics.Comment: 23 pages, 10 figure

Stretching and heating cells with light - Nonlinear photothermal cell rheology

Stretching and heating are everyday experiences for skin and tissue cells. They are also standard procedures to reduce the risk for injuries in physical exercise and to relieve muscle spasms in physiotherapy. Here, we ask which immediate and long-term mechanical effects of such treatments are quantitatively detectable on the level of individual living cells. Combining versatile optical stretcher techniques with a well-tested mathematical model for viscoelastic polymer networks, we investigate the thermomechanical properties of suspended cells with a photothermal rheometric protocol that can disentangle fast transient and slow 'inelastic' components in the nonlinear mechanical response. We find that a certain minimum strength and duration of combined stretching and heating is required to induce long-lived alterations of the mechanical state of the cells, which then respond qualitatively differently to mechanical tests than after weaker/shorter treatments or merely mechanical preconditioning alone. Our results suggest a viable protocol to search for intracellular biomolecular signatures of the mathematically detected dissimilar mechanical response modes. © 2020 The Author(s). Published by IOP Publishing Ltd on behalf of the Institute of Physics and Deutsche Physikalische Gesellschaft

Dissection of the Inflammatory Bowel Disease Transcriptome Using Genome-Wide cDNA Microarrays

BACKGROUND: The differential pathophysiologic mechanisms that trigger and maintain the two forms of inflammatory bowel disease (IBD), Crohn disease (CD), and ulcerative colitis (UC) are only partially understood. cDNA microarrays can be used to decipher gene regulation events at a genome-wide level and to identify novel unknown genes that might be involved in perpetuating inflammatory disease progression. METHODS AND FINDINGS: High-density cDNA microarrays representing 33,792 UniGene clusters were prepared. Biopsies were taken from the sigmoid colon of normal controls (n = 11), CD patients (n = 10) and UC patients (n = 10). (33)P-radiolabeled cDNA from purified poly(A)(+) RNA extracted from biopsies (unpooled) was hybridized to the arrays. We identified 500 and 272 transcripts differentially regulated in CD and UC, respectively. Interesting hits were independently verified by real-time PCR in a second sample of 100 individuals, and immunohistochemistry was used for exemplary localization. The main findings point to novel molecules important in abnormal immune regulation and the highly disturbed cell biology of colonic epithelial cells in IBD pathogenesis, e.g., CYLD (cylindromatosis, turban tumor syndrome) and CDH11 (cadherin 11, type 2). By the nature of the array setup, many of the genes identified were to our knowledge previously uncharacterized, and prediction of the putative function of a subsection of these genes indicate that some could be involved in early events in disease pathophysiology. CONCLUSION: A comprehensive set of candidate genes not previously associated with IBD was revealed, which underlines the polygenic and complex nature of the disease. It points out substantial differences in pathophysiology between CD and UC. The multiple unknown genes identified may stimulate new research in the fields of barrier mechanisms and cell signalling in the context of IBD, and ultimately new therapeutic approaches