Automating Deductive Verification for Weak-Memory Programs

Writing correct programs for weak memory models such as the C11 memory model is challenging because of the weak consistency guarantees these models provide. The first program logics for the verification of such programs have recently been proposed, but their usage has been limited thus far to manual proofs. Automating proofs in these logics via first-order solvers is non-trivial, due to reasoning features such as higher-order assertions, modalities and rich permission resources. In this paper, we provide the first implementation of a weak memory program logic using existing deductive verification tools. We tackle three recent program logics: Relaxed Separation Logic and two forms of Fenced Separation Logic, and show how these can be encoded using the Viper verification infrastructure. In doing so, we illustrate several novel encoding techniques which could be employed for other logics. Our work is implemented, and has been evaluated on examples from existing papers as well as the Facebook open-source Folly library.Comment: Extended version of TACAS 2018 publicatio

Nomad DNA — A model for movement and duplication of DNA sequences in plant genomes

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/43425/1/11103_2004_Article_BF00019160.pd

Mid-infrared supercontinuum-based Fourier transform spectroscopy for plasma analysis

Broadband mid-infrared (MIR) spectroscopy is a well-established and valuable diagnostic technique for reactive plasmas. Plasmas are complex systems and consist of numerous (reactive) types of molecules; it is challenging to measure and control reaction specificity with a good sensitivity. Here, we demonstrate the first use of a novel MIR supercontinuum (SC) source for quantitative plasma spectroscopy. The SC source has a wide spectral coverage of 1300-2700 cm−1 (wavelength range 3.7-7.7 μm), thus enabling broadband multispecies detection. The high spatial coherence of the MIR SC source provides long interaction path lengths, thereby increasing the sensitivity for molecular species. The combination of such a SC source with a custom-built FTIR spectrometer (0.1 cm−1 spectral resolution) allows detection of various gases with high spectral resolution. We demonstrate its potential in plasma applications by accurate identification and quantification of a variety of reaction products (e.g. nitrogen oxides and carbon oxides) under low-pressure conditions, including the molecular species with overlapping absorbance features (e.g. acetone, acetaldehyde, formaldehyde, etc.).<br/

IFN-γ-induced PD-L1 expression on human melanocytes is impaired in vitiligo

Mounting evidence shows that the PD-1/PD-L1 axis is involved in tumor immune evasion. This is demonstrated by anti-PD-1 antibodies that can reverse tumor-associated PD-L1 to functionally suppress anti-tumor T-cell responses. Since type I and II interferons are key regulators of PD-L1 expression in melanoma cells and IFN-γ-producing CD8+ T cells and IFN-α-producing dendritic cells are abundant in vitiligo skin, we aimed to study the role of PD-1/PD-L1 signalling in melanocyte destruction in vitiligo. Moreover, impaired PD-1/PD-L1 function is observed in a variety of autoimmune diseases. It is, therefore, hypothesized that manipulating PD-1/PD-L1 signalling might have therapeutic potential in vitiligo. The PD-1+ T cells were abundantly present in situ in perilesional vitiligo skin, but expression of PD-L1 was limited and confined exclusively to dermal T cells. More specifically, neither melanocytes nor other epidermal skin cells expressed PD-L1. Exposure to IFN-γ, but also type I interferons, increased PD-L1 expression in primary melanocytes and fibroblasts, derived from healthy donors. Primary human keratinocytes only showed increased PD-L1 expression upon stimulation with IFN-γ. More interestingly, melanocytes derived from non-lesional vitiligo skin showed no PD-L1 upregulation upon IFN-γ exposure, while other skin cells displayed significant PD-L1 expression after exposure. In a vitiligo skin explant model, incubation of non-lesional vitiligo skin with activated (IFN-γ-producing) T cells from vitiligo lesions was previously described to induce melanocyte apoptosis. Although PD-L1 expression was induced in epidermal cells in these explants, this induction was completely absent in melanocytes. The lack of PD-L1 upregulation by melanocytes in the presence of IFN-γ-producing T cells shows that melanocytes lack protection against T-cell attack during vitiligo pathogenesis. Manipulating PD-1/PD-L1 signalling may, therefore, be a therapeutic option for vitiligo patients