Perovskites have been demonstrated in solar cells with power conversion efficiency well above 20%, which makes them one of the strongest contenders for the next generation photovoltaics. While there are no concerns about their efficiency, very little is known about their stability under illumination and load. Ionic defects and their migration in the perovskite crystal lattice are one of the most alarming sources of degradation, which can potentially prevent the commercialization of perovskite solar cells (PSCs). In this work, we provide direct evidence of electric field-induced ionic defect migration and we isolate their effect on the long-term performance of state-of-the-art devices. Supported by modelling, we demonstrate that ionic defects, migrating on timescales significantly longer (above 10 3 s) than what has so far been explored (from 10 -1 to 10 2 s), abate the initial efficiency by 10-15% after several hours of operation at the maximum power point. Though these losses are not negligible, we prove that the initial efficiency is fully recovered when leaving the device in the dark for a comparable amount of time. We verified this behaviour over several cycles resembling day/night phases, thus probing the stability of PSCs under native working conditions. This unusual behaviour reveals, that research and industrial standards currently in use to assess the performance and the stability of solar cells need to be adjusted for PSCs.Our work paves the way towards much needed new testing protocols and figures of merit specifically designed for PSCs.4

We have developed a charge transport model that explicitly accounts for ion migration. This model has been used to interpret measured current–voltage characteristics that show hysteresis.

Hybrid perovskites represent a new paradigm for photovoltaics, which have the potential to overcome the performance limits of current technologies and achieve low cost and high versatility. However, an efficiency drop is often observed within the first few hundred hours of device operation, which could become an important issue. Here, we demonstrate that the electrode's metal migrating through the hole transporting material (HTM) layer and eventually contacting the perovskite is in part responsible for this early device degradation. We show that depositing the HTM within an insulating mesoporous "buffer layer" comprised of Al2O3 nanoparticles prevents the metal electrode migration while allowing for precise control of the HTM thickness. This enables an improvement in the solar cell fill factor and prevents degradation of the device after 350 h of operation.

The effects of transport layers on perovskite solar cell performance, in particular anomalous hysteresis, are investigated.

The human brain is the organ with the highest metabolic activity but it lacks a traditional lymphatic system responsible for clearing waste products. We have demonstrated that the basement membranes of cerebral capillaries and arteries represent the lymphatic pathways of the brain along which intramural periarterial drainage (IPAD) of soluble metabolites occurs. Failure of IPAD could explain the vascular deposition of the amyloid-beta protein as cerebral amyloid angiopathy (CAA), which is a key pathological feature of Alzheimer's disease. The underlying mechanisms of IPAD, including its motive force, have not been clarified, delaying successful therapies for CAA. Although arterial pulsations from the heart were initially considered to be the motive force for IPAD, they are not strong enough for efficient IPAD. This study aims to unravel the driving force for IPAD, by shifting the perspective of a heart-driven clearance of soluble metabolites from the brain to an intrinsic mechanism of cerebral arteries (e.g., vasomotion-driven IPAD). We test the hypothesis that the cerebrovascular smooth muscle cells, whose cycles of contraction and relaxation generate vasomotion, are the drivers of IPAD. A novel multiscale model of arteries, in which we treat the basement membrane as a fluid-filled poroelastic medium deformed by the contractile cerebrovascular smooth muscle cells, is used to test the hypothesis. The vasomotion-induced intramural flow rates suggest that vasomotion-driven IPAD is the only mechanism postulated to date capable of explaining the available experimental observations. The cerebrovascular smooth muscle cells could represent valuable drug targets for prevention and early interventions in CAA.

A mathematical model for targeted drug delivery using magnetic particles is developed. This includes a diffusive flux of particles arising from interactions between erythrocytes in the microcirculation. The model is used to track particles in a vessel network. Magnetic field design is discussed and we show that it is impossible to specifically target internal regions using an externally applied field. r

The drying process is a crucial step in electrode manufacture that may lead to spatial inhomogeneities in the distribution of the electrode components resulting in impaired cell performance. Binder migration during the drying process, and the ensuing poor binder coverage in certain regions of the electrode, can lead to capacity fade and mechanical failure (e.g. electrode delamination from the current collector). A mathematical model of electrode drying is presented which tracks the evolution of the binder distribution, and is applicable in the relatively high drying rates encountered in industrial electrode manufacture. The model predicts that constant low drying rates lead to a favourable homogeneous binder profiles, whereas constant high drying rates are unfavourable and result in accumulation of binder near the evaporation surface and depletion near the current collector. These results show strong qualitative agreement with experimental observations and provide a cogent explanation for why fast drying conditions result in poorly performing electrodes. Finally, a scheme is detailed for optimisation of a time-varying drying procedure that allows for short drying times whilst simultaneously ensuring a close to homogeneous binder distribution throughout the electrode.

Tumor hypoxia is associated with low rates of cell proliferation and poor drug delivery, limiting the efficacy of many conventional therapies such as chemotherapy. Because many macrophages accumulate in hypoxic regions of tumors, one way to target tumor cells in these regions could be to use genetically engineered macrophages that express therapeutic genes when exposed to hypoxia. Systemic delivery of such therapeutic macrophages may also be enhanced by preloading them with nanomagnets and applying a magnetic field to the tumor site. Here, we use a new mathematical model to compare the effects of conventional cyclophosphamide therapy with those induced when macrophages are used to deliver hypoxia-inducible cytochrome P450 to locally activate cyclophosphamide. Our mathematical model describes the spatiotemporal dynamics of vascular tumor growth and treats cells as distinct entities. Model simulations predict that combining conventional and macrophagebased therapies would be synergistic, producing greater antitumor effects than the additive effects of each form of therapy. We find that timing is crucial in this combined approach with efficacy being greatest when the macrophage-based, hypoxia-targeted therapy is administered shortly before or concurrently with chemotherapy. Last, we show that therapy with genetically engineered macrophages is markedly enhanced by using the magnetic approach described above, and that this enhancement depends mainly on the strength of the applied field, rather than its direction. This insight may be important in the treatment of nonsuperficial tumors, where generating a specific orientation of a magnetic field may prove difficult. In conclusion, we demonstrate that mathematical modeling can be used to design and maximize the efficacy of combined therapeutic approaches in cancer. Cancer Res; 71(8); 2826-37. Ó2011 AACR.