Controlled Dephasing of a Quantum Dot: From Coherent to Sequential Tunneling

Resonant tunneling through identical potential barriers is a textbook problem in quantum mechanics. Its solution yields total transparency (100% tunneling) at discrete energies. This dramatic phenomenon results from coherent interference among many trajectories, and it is the basis of transport through periodic structures. Resonant tunneling of electrons is commonly seen in semiconducting 'quantum dots'. Here we demonstrate that detecting (distinguishing) electron trajectories in a quantum dot (QD) renders the QD nearly insulating. We couple trajectories in the QD to a 'detector' by employing edge channels in the integer quantum Hall regime. That is, we couple electrons tunneling through an inner channel to electrons in the neighboring outer, 'detector' channel. A small bias applied to the detector channel suffices to dephase (quench) the resonant tunneling completely. We derive a formula for dephasing that agrees well with our data and implies that just a few electrons passing through the detector channel suffice to dephase the QD completely. This basic experiment shows how path detection in a QD induces a transition from delocalization (due to coherent tunneling) to localization (sequential tunneling)

Observational cohort study of IP-10's potential as a biomarker to aid in inflammation regulation within a clinical decision support protocol for patients with severe COVID-19.

BackgroundTreatment of severely ill COVID-19 patients requires simultaneous management of oxygenation and inflammation without compromising viral clearance. While multiple tools are available to aid oxygenation, data supporting immune biomarkers for monitoring the host-pathogen interaction across disease stages and for titrating immunomodulatory therapy is lacking.MethodsIn this single-center cohort study, we used an immunoassay platform that enables rapid and quantitative measurement of interferon γ-induced protein 10 (IP-10), a host protein involved in lung injury from virus-induced hyperinflammation. A dynamic clinical decision support protocol was followed to manage patients infected with severe acute respiratory syndrome coronavirus 2 and examine the potential utility of timely and serial measurements of IP-10 as tool in regulating inflammation.ResultsOverall, 502 IP-10 measurements were performed on 52 patients between 7 April and 10 May 2020, with 12 patients admitted to the intensive care unit. IP-10 levels correlated with COVID-19 severity scores and admission to the intensive care unit. Among patients in the intensive care unit, the number of days with IP-10 levels exceeding 1,000 pg/mL was associated with mortality. Administration of corticosteroid immunomodulatory therapy decreased IP-10 levels significantly. Only two patients presented with subsequent IP-10 flare-ups exceeding 1,000 pg/mL and died of COVID-19-related complications.ConclusionsSerial and readily available IP-10 measurements potentially represent an actionable aid in managing inflammation in COVID-19 patients and therapeutic decision-making.Trial registrationClinicaltrials.gov, NCT04389645, retrospectively registered on May 15, 2020