357 research outputs found

    How (Not) to Index Order Revealing Encrypted Databases

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    Order Reveling Encryption (ORE) enables efficient range queries on encrypted databases, but may leak information that could be exploited by inference attacks. State-of-the-art ORE schemes claim different security guarantees depending on the adversary attack surface. Intuitively, online adversaries who access the database server at runtime may access information leakage; offline adversaries who access only a snapshot of the database data should not be able to gain useful information. We focus on offline security of the ORE scheme proposed by Lewi and Wu (LW-ORE, CCS 2016), which guarantees semantic security of ciphertexts stored in the database, but requires that ciphertexts are maintained sorted with regard to the corresponding plaintexts to support sublinear time queries. The design of LW-ORE does not discuss how to build indexing data structures to maintain sorting. The risk is that practitioners consider indexes as a technicality whose design does not affect security. We show that indexes can affect offline security of LW-ORE because they may leak duplicate plaintext values, and statistical information on plaintexts distribution and on transactions history. As a real-world demonstration, we found two open source implementations related to academic research (JISA 2018, VLDB 2019), and both adopt standard search trees which may introduce such vulnerabilities. We discuss necessary conditions for indexing data structures to be secure for ORE databases, and we outline practical solutions. Our analyses could represent an insightful lesson in the context of security failures due to gaps between theoretical modeling and actual implementation, and may also apply to other cryptographic techniques for securing outsourced databases

    Smurf2 regulates hematopoietic stem cell self-renewal and aging

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    The age-dependent decline in the self-renewal capacity of stem cells plays a critical role in aging, but the precise mechanisms underlying this decline are not well understood. By limiting proliferative capacity, senescence is thought to play an important role in age-dependent decline of stem cell self-renewal, although direct evidence supporting this hypothesis is largely lacking. We have previously identified the E3 ubiquitin ligase Smurf2 as a critical regulator of senescence. In this study, we found that mice deficient in Smurf2 had an expanded hematopoietic stem cell (HSC) compartment in bone marrow under normal homeostatic conditions, and this expansion was associated with enhanced proliferation and reduced quiescence of HSCs. Surprisingly, increased cycling and reduced quiescence of HSCs in Smurf2-deficient mice did not lead to premature exhaustion of stem cells. Instead, HSCs in aged Smurf2-deficient mice had a significantly better repopulating capacity than aged wild-type HSCs, suggesting that decline in HSC function with age is Smurf2 dependent. Furthermore, Smurf2-deficient HSCs exhibited elevated long-term self-renewal capacity and diminished exhaustion in serial transplantation. As we found that the expression of Smurf2 was increased with age and in response to regenerative stress during serial transplantation, our findings suggest that Smurf2 plays an important role in regulating HSC self-renewal and aging

    A case of cryptogenic organizing pneumonia occurring in Crohn's disease.

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    A 29 year-old-man with Crohn's disease, who developed diffuse pulmonary infiltrates and hypoxemia two months following oral administration of mesalazine, was examined. Clinical findings and computed tomography were suggestive of, and lung histology was diagnostic of, bronchiolitis obliterans organizing pneumonia, also known as cryptogenic organizing pneumonia. Although the data did not allow for definitive conclusions, they did suggest that the pulmonary disease was an extraintestinal manifestation of Crohn's disease, rather than an adverse reaction to mesalazine. In fact, the patient showed clinical, radiological and functional improvements, despite the treatment with mesalazine and the withdrawal of steroid therapy

    A kingdom in decline. Holocene range contraction of the lion (Panthera leo) modelled with Global Environmental Stratification

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    Aim We use ecological niche models and environmental stratification of palaeoclimate to reconstruct the changing range of the lion (Panthera leo) during the late Pleistocene and Holocene. Location The modern (early 21st century) range of the lion extends from southern Africa to the western Indian Subcontinent, yet through the 20th century this range has been drastically reduced in extent and become increasingly fragmented as a result of human impacts. Methods We use Global Environmental Stratification with MaxEnt ecological niche models to map environmental suitability of the lion under current and palaeoclimatic scenarios. By examining modelled lion range in terms of categorical environmental strata, we characterise suitable bioclimatic conditions for the lion in a descriptive manner. Results We find that lion habitat suitability has reduced throughout the Holocene, controlled by pluvial/interpluvial cycles. The aridification of the Sahara 6ka dramatically reduced lion range throughout North Africa. The association of Saharan aridification with the development of pastoralism and the growth of sedentary communities, who practised animal husbandry, would have placed additional and lasting anthropogenic pressures on the lion. Main Conclusions This research highlights the need to integrate the full effects of the fluctuating vegetation and desiccation of the Sahara into palaeoclimatic models, and provides a starting point for further continental-scale analyses of shifting faunal ranges through North Africa and the Near East during the Holocene. This scale of ecological niche modelling does not explain the current pattern of genetic variation in the lion, and we conclude that narrow but substantial physical barriers, such as rivers, have likely played a major role in population vicariance throughout the Late Pleistocene

    Inhibition of Bromodomain Proteins in Treatment of Diffuse Large B-cell Lymphoma

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    Only ~50% of patients with diffuse large B-cell lymphoma (DLBCL), the most common and aggressive subtype of non-Hodgkin’s lymphoma, enter long-term remission after standard chemotherapy, and patients who do not respond to treatment have few options. Therefore, there is a critical need for effective and targeted therapeutics for DLBCL. Recent studies highlight the incidence of increased c-MYC protein in DLBCL and the correlation between high levels of c-MYC and poor survival prognosis of DLBCL patients, suggesting that c-MYC is a compelling therapeutic target for DLBCL therapy. The small molecule JQ1 suppresses c-MYC expression through inhibition of the BET family of bromodomain proteins. We show that JQ1 efficiently inhibited cell proliferation of human DLBCL cells regardless of their molecular subtypes, suggesting a broad effect of JQ1 in DLBCL. After JQ1 treatment, initial G1 arrest in DLBCL cells was followed by either apoptosis or senescence. In DLBCL cells treated with JQ1, we found that c-MYC expression was suppressed in the context of the natural, chromosomally-translocated or an amplified gene locus. Furthermore, JQ1 treatment significantly suppressed growth of DLBCL cells engrafted subcutaneously and improved survival of mice engrafted with DLBCL cells intraperitoneally. These results demonstrate that inhibition of the BET family of bromodomain proteins, and consequently c-MYC, has the potential clinical utility in DLBCL treatment
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