Lattice-Based Group Signatures: Achieving Full Dynamicity (and Deniability) with Ease

In this work, we provide the first lattice-based group signature that offers full dynamicity (i.e., users have the flexibility in joining and leaving the group), and thus, resolve a prominent open problem posed by previous works. Moreover, we achieve this non-trivial feat in a relatively simple manner. Starting with Libert et al.'s fully static construction (Eurocrypt 2016) - which is arguably the most efficient lattice-based group signature to date, we introduce simple-but-insightful tweaks that allow to upgrade it directly into the fully dynamic setting. More startlingly, our scheme even produces slightly shorter signatures than the former, thanks to an adaptation of a technique proposed by Ling et al. (PKC 2013), allowing to prove inequalities in zero-knowledge. Our design approach consists of upgrading Libert et al.'s static construction (EUROCRYPT 2016) - which is arguably the most efficient lattice-based group signature to date - into the fully dynamic setting. Somewhat surprisingly, our scheme produces slightly shorter signatures than the former, thanks to a new technique for proving inequality in zero-knowledge without relying on any inequality check. The scheme satisfies the strong security requirements of Bootle et al.'s model (ACNS 2016), under the Short Integer Solution (SIS) and the Learning With Errors (LWE) assumptions. Furthermore, we demonstrate how to equip the obtained group signature scheme with the deniability functionality in a simple way. This attractive functionality, put forward by Ishida et al. (CANS 2016), enables the tracing authority to provide an evidence that a given user is not the owner of a signature in question. In the process, we design a zero-knowledge protocol for proving that a given LWE ciphertext does not decrypt to a particular message

Deletion of diacylglycerol-responsive TRPC genes attenuates diabetic nephropathy by inhibiting activation of the TGFβ1 signaling pathway

TRPC6 plays a critical role in proteinuric kidney diseases, and TRPC3 is involved in tubulointerstitialdamage and renal fibrosis in obstructed kidneys. Podocyte loss is a characteristic event in diabetic nephropathy(DN). The aim of this study was to examine whether deletion of the closely related diacylglycerol (DAG)-responsiveTRPCs in mice (TRPC3/6/7-/-) affects diabetes-induced renal dysfunction and podocyte loss. We compared urinevolume, kidney hypertrophy, glomerular enlargement, albuminuria and podocyte loss between wild type (WT) andTRPC3/6/7-/- diabetic mice. Finally, we examined whether the TGFβ1 signaling pathway is changed in diabetic WTand TRPC3/6/7-/- mice. TRPC6 protein in the renal cortex was increased in WT diabetic mice. High glucose (HG)treatment increased TRPC6 expression in human podocytes. TRPC3 protein, however, was not altered in eitherdiabetic mice or HG-treated human podocytes. Although diabetic WT and TRPC3/6/7-/- mice had similar levels ofhyperglycemia, the TRPC3/6/7-/- diabetic mice showed less polyuria, kidney hypertrophy, glomerular enlargement,albuminuria, and had lost less podocytes compared with WT diabetic mice. In addition, we observed decreasedexpression of anti-apoptotic Bcl2 and increased expression of pro-apoptotic cleaved caspase 3 in WT diabetic mice,but such changes were not significant in TRPC3/6/7-/- diabetic mice. Western blot and immunohistochemistry revealedthat TGFβ1, p-Smad2/3, and fibronectin were upregulated in WT diabetic mice; however, expression of thesesignaling molecules was not changed in TRPC3/6/7-/- diabetic mice. In conclusion, deletion of DAG-responsiveTRPCs attenuates diabetic renal injury via inhibiting the upregulation of TGFβ1 signaling in diabetic kidneys.Fil: Liu, Benju. Huazhong University of Science and Technology; ChinaFil: He, Xiju. Huazhong University of Science and Technology; ChinaFil: Li, Shoutian. Yangtze University; ChinaFil: Xu, Benke. Yangtze University; ChinaFil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; ArgentinaFil: Liao, Yanhong. Huazhong University of Science and Technology; Chin

AZI23'UTR Is a New SLC6A3 Downregulator Associated with an Epistatic Protection Against Substance Use Disorders

Regulated activity of SLC6A3, which encodes the human dopamine transporter (DAT), contributes to diseases such as substance abuse disorders (SUDs); however, the exact transcription mechanism remains poorly understood. Here, we used a common genetic variant of the gene, intron 1 DNP1B sequence, as bait to screen and clone a new transcriptional activity, AZI23'UTR, for SLC6A3. AZI23'UTR is a 3' untranslated region (3'UTR) of the human 5-Azacytidine Induced 2 gene (AZI2) but appeared to be transcribed independently of AZI2. Found to be present in both human cell nuclei and dopamine neurons, this RNA was shown to downregulate promoter activity through a variant-dependent mechanism in vitro. Both reduced RNA density ratio of AZI23'UTR/AZI2 and increased DAT mRNA levels were found in ethanol-naive alcohol-preferring rats. Secondary analysis of dbGaP GWAS datasets (Genome-Wide Association Studies based on the database of Genotypes and Phenotypes) revealed significant interactions between regions upstream of AZI23'UTR and SLC6A3 in SUDs. Jointly, our data suggest that AZI23'UTR confers variant-dependent transcriptional regulation of SLC6A3, a potential risk factor for SUDs

Transmission of H7N9 influenza virus in mice by different infective routes.

BackgroundOn 19 February 2013, the first patient infected with a novel influenza A H7N9 virus from an avian source showed symptoms of sickness. More than 349 laboratory-confirmed cases and 109 deaths have been reported in mainland China since then. Laboratory-confirmed, human-to-human H7N9 virus transmission has not been documented between individuals having close contact; however, this transmission route could not be excluded for three families. To control the spread of the avian influenza H7N9 virus, we must better understand its pathogenesis, transmissibility, and transmission routes in mammals. Studies have shown that this particular virus is transmitted by aerosols among ferrets.MethodsTo study potential transmission routes in animals with direct or close contact to other animals, we investigated these factors in a murine model.ResultsViable H7N9 avian influenza virus was detected in the upper and lower respiratory tracts, intestine, and brain of model mice. The virus was transmissible between mice in close contact, with a higher concentration of virus found in pharyngeal and ocular secretions, and feces. All these biological materials were contagious for naïve mice.ConclusionsOur results suggest that the possible transmission routes for the H7N9 influenza virus were through mucosal secretions and feces

A study of health effects of long-distance ocean voyages on seamen using a data classification approach

Background: Long-distance ocean voyages may have substantial impacts on seamen’s health, possibly causing malnutrition and other illness. Measures can possibly be taken to prevent such problems from happening through preparing special diet and making special precautions prior or during the sailing if a detailed understanding can be gained about what specific health effects such voyages may have on the seamen. Methods: We present a computational study on 200 seamen using 41 chemistry indicators measured on their blood samples collected before and after the sailing. Our computational study is done using a data classification approach with a support vector machine-based classifier in conjunction with feature selections using a recursive feature elimination procedure. Results: Our analysis results suggest that among the 41 blood chemistry measures, nine are most likely to be affected during the sailing, which provide important clues about the specific effects of ocean voyage on seamen’s health. Conclusions: The identification of the nine blood chemistry measures provides important clues about the effects of long-distance voyage on seamen’s health. These findings will prove to be useful to guide in improving the living and working environment, as well as food preparation on ships

The mouse and ferret models for studying the novel avian-origin human influenza A (H7N9) virus.

BackgroundThe current study was conducted to establish animal models (including mouse and ferret) for the novel avian-origin H7N9 influenza virus.FindingsA/Anhui/1/2013 (H7N9) virus was administered by intranasal instillation to groups of mice and ferrets, and animals developed typical clinical signs including body weight loss (mice and ferrets), ruffled fur (mice), sneezing (ferrets), and death (mice). Peak virus shedding from respiratory tract was observed on 2 days post inoculation (d.p.i.) for mice and 3-5 d.p.i. for ferrets. Virus could also be detected in brain, liver, spleen, kidney, and intestine from inoculated mice, and in heart, liver, and olfactory bulb from inoculated ferrets. The inoculation of H7N9 could elicit seroconversion titers up to 1280 in ferrets and 160 in mice. Leukopenia, significantly reduced lymphocytes but increased neutrophils were also observed in mouse and ferret models.ConclusionsThe mouse and ferret model enables detailed studies of the pathogenesis of this illness and lay the foundation for drug or vaccine evaluation