We show the incorporation of europium into CsPbI 2 Br inorganic perovskite lattice. With the optimization of the doping concentration of europium, we obtained a high power-conversion efficiency of 13.71%. We found that incorporation of europium reduces non-radiative recombination to achieve a high open-circuit voltage of 1.27 V. The exceptional stability of such a device was demonstrated by retaining 93% of the initial efficiency under 100 mW cm À2 continuous illumination for 370 hr.

We demonstrated a high-sensitivity strain sensor based on an in-fiber Fabry-Perot interferometer (FPI) with an air cavity, which was created by splicing together two sections of standard single-mode fibers. The sensitivity of this strain sensor was enhanced to 6.0  pm/με by improving the cavity length of the FPI by means of repeating arc discharges for reshaping the air cavity. Moreover, such a strain sensor has a very low temperature sensitivity of 1.1  pm/°C, which reduces the cross sensitivity between tensile strain and temperature.

We demonstrated a unique rectangular air bubble by means of splicing two sections of standard single mode fibers together and tapering the splicing joint. Such an air bubble can be used to develop a promising high-sensitivity strain sensor based on Fabry-Perot interference. The sensitivity of the strain sensor with a cavity length of about 61 μm and a wall thickness of about 1 μm was measured to be up to 43.0 pm/με and is the highest strain sensitivity among the in-fiber FPI-based strain sensors with air cavities reported so far. Moreover, our strain sensor has a very low temperature sensitivity of about 2.0 pm/°C. Thus, the temperature-induced strain measurement error is less than 0.046 με/°C.

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COVID-19 is primarily known as a respiratory disease caused by SARS-CoV-2. However, neurological symptoms such as memory loss, sensory confusion, severe headaches, and even stroke are reported in up to 30% of cases and can persist even after the infection is over (long COVID). These neurological symptoms are thought to be produced by the virus infecting the central nervous system, however we don’t understand the molecular mechanisms triggering them. The neurological effects of COVID-19 share similarities to neurodegenerative diseases in which the presence of cytotoxic aggregated amyloid protein or peptides is a common feature. Following the hypothesis that some neurological symptoms of COVID-19 may also follow an amyloid etiology we identified two peptides from the SARS-CoV-2 proteome that self-assemble into amyloid assemblies. Furthermore, these amyloids were shown to be highly toxic to neuronal cells. We suggest that cytotoxic aggregates of SARS-CoV-2 proteins may trigger neurological symptoms in COVID-19.