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Ruddlesden–Popper halide perovskites are 2D solution-processed quantum wells with a general formula A 2 A’ n -1 M n X 3 n +1 , where optoelectronic properties can be tuned by varying the perovskite layer thickness ( n -value), and have recently emerged as efficient semiconductors with technologically relevant stability. However, fundamental questions concerning the nature of optical resonances (excitons or free carriers) and the exciton reduced mass, and their scaling with quantum well thickness, which are critical for designing efficient optoelectronic devices, remain unresolved. Here, using optical spectroscopy and 60-Tesla magneto-absorption supported by modeling, we unambiguously demonstrate that the optical resonances arise from tightly bound excitons with both exciton reduced masses and binding energies decreasing, respectively, from 0.221  m 0 to 0.186  m 0 and from 470 meV to 125 meV with increasing thickness from n equals 1 to 5. Based on this study we propose a general scaling law to determine the binding energy of excitons in perovskite quantum wells of any layer thickness. Hybrid 2D layered perovskites are solution-processed quantum wells whose optoelectronic properties are tunable by varying the thickness of the inorganic slab. Here Blancon et al. work out a general behavior for dependence of the excitonic properties in layered 2D perovskites.

We have observed photoinduced negative optical conductivity, or gain, in the terahertz frequency range in a GaAs multiple-quantum-well structure in a strong perpendicular magnetic field at low temperatures. The gain is narrow-band: it appears as a sharp peak (linewidth \\(<\\)0.45 meV) whose frequency shifts with applied magnetic field. The gain has a circular-polarization selection rule: a strong line is observed for hole-cyclotron-resonance-active polarization. Furthermore, the gain appears only when the exciton \\(1s\\) state is populated, which rules out intraexcitonic transitions to be its origin. Based on these observations, we propose a possible process in which the stimulated emission of a terahertz photon occurs while two free excitons scatter into one biexciton in an energy and angular-momentum conserving manner.

Primary immune thrombocytopenia is an autoimmune disorder mediated partly by platelet autoantibodies, resulting in thrombocytopenia, bleeding, and constitutional symptoms. Efgartigimod, a first-in-class novel human IgG1 Fc fragment, binds the neonatal Fc receptor with high affinity and thus reduces serum IgG concentrations, including autoantibodies. The objective of this study was to evaluate the efficacy and safety of efgartigimod in adults with persistent and chronic primary immune thrombocytopenia. This phase 3, multicentre, randomised, double-blinded, placebo-controlled, 24-week study evaluated the efficacy and safety of intravenous efgartigimod in adults aged 18 years or older with chronic or persistent primary immune thrombocytopenia who had an average platelet count of less than 30 000, had responded to at least one previous immune thrombocytopenia therapy, and were on a concurrent therapy at baseline or had received at least a second previous immune thrombocytopenia therapy. The study took place in 71 participating sites from Asia, Europe, and North America. Patients were randomly assigned 2:1 to receive either efgartigimod (10 mg/kg) or placebo intravenously for the first 4 weeks, after which the dosing schedule could be altered to once per week or every other week depending on the patients' platelet count. The primary endpoint, evaluated in the chronic population, was sustained platelet count response (≥50 × 109 for at least 4 of the last 6 weeks). This study is registered with ClinicalTrials.gov (NCT04188379) and is completed. A total of 205 patients were screened from Dec 9, 2019, to Feb 3, 2022, and 131 (86 in the efgartigimod group; 45 in the placebo group) were randomly assigned. These patients represented a population with long-term disease who had a mean time since diagnosis of 10·6 years and 67% (88/131) of whom had received at least three previous immune thrombocytopenia treatments. 22% (17/78) of patients with chronic immune thrombocytopenia receiving efgartigimod reached the primary endpoint compared with 5% (2/40) of those receiving placebo (p=0·032; adjusted difference in response, 16% [95% CI 2·6–26·4]). The median number of weeks of disease control in patients with chronic immune thrombocytopenia was 2·0 (IQR 0·0–11·0) for efgartigimod versus 0·0 (0·0–1·0) for placebo (p=0·0009). Efgartigimod was well tolerated; most adverse events were mild to moderate in severity. The most common adverse events of interest in both groups were headache (16% in efgartigimod and 13% in placebo), haematuria (16% in efgartigimod and 16% in placebo), and petechiae (15% in efgartigimod and 27% in placebo). Efgartigimod significantly increased sustained platelet count responses compared with placebo in patients with chronic immune thrombocytopenia, including those who had received multiple previous immune thrombocytopenia therapies. Upon completion of the ADVANCE IV study, patients could enroll in the ongoing open-label extension. Subcutaneous efgartigimod is currently being evaluated in patients with immune thrombocytopenia in the ADVANCE SC+ trial. argenx.