Mining CryptoNight-Haven on the Varium C1100 Blockchain Accelerator Card

Cryptocurrency mining is an energy-intensive process that presents a prime candidate for hardware acceleration. This work-in-progress presents the first coprocessor design for the ASIC-resistant CryptoNight-Haven Proof of Work (PoW) algorithm. We construct our hardware accelerator as a Xilinx Run Time (XRT) RTL kernel targeting the Xilinx Varium C1100 Blockchain Accelerator Card. The design employs deeply pipelined computation and High Bandwidth Memory (HBM) for the underlying scratchpad data. We aim to compare our accelerator to existing CPU and GPU miners to show increased throughput and energy efficiency of its hash computation

Neutrophils play a key role in the initiation of glomerular hematuria in a postinfectious igan experimental model

2 p.BACKGROUND AND AIMS: Hematuria is a common finding in patients with IgA nephropathy (IgAN), occurring mainly after upper respiratory tract infections.Hematuria can lead to acute kidney injury and chronic loss of renal function in IgAN.However, the mechanisms involved in egression of erythrocytes from the glomerular capillaries into the urinary space are unknown. To answer this question, we developed an infection with Streptococcus pneumoniae (SP) in a humanized experimental IgAN model (a1KICD89tg mice) that resembles the pathological and clinical findings of disease (IgA1 and soluble CD89 mesangial deposits, complement activation,proteinuria and hematuria).METHOD: a1KICD89tg mice (12 weeks old) received an intranasal instillation of SP(107 bacteria). Blood, urine and renal samples were obtained during 1 month after induction of respiratory infection. The presence of SP in lungs from these mice was confirmed by microbiological analysis. Hematuria was quantified in the urinary sediment and renal function was determined by biochemical analysis. Renal histological characteristics were evaluated by hematoxylin/eosin, masson’s trichrome and PAS staining. IgA glomerular deposits, activation of complement system and infiltration of proinflammatory cells was examined by immunohistochemistry or immunofluorescence. Circulating leukocyte populations were studied on a hemocytometer. Renal inflammatory cytokines, metalloproteases, as well as markers of tubular and glomerular damage were determined in kidneys by RT-PCR and western-blot. To further validate the role of neutrophils in this pathological setting, we selective depleted these cells through a single injection of anti-Ly6G mAb (200 mg/kg i.p).RESULTS: SP-intranasal instillation in a1KICD89tg mice increased hematuria,microalbuminuria and proteinuria, peaking at 48h after induction of the respiratory infection. SP instillation caused disruption of the glomerular basement membrane,with decreased expression of the slit diaphragm proteins nephrin and synaptopodin, as well as higher glomerular accumulation of IgA and proteins of complement system (C3, MBL). Hematuria intensity was positively correlated with the presence of interstitial F4/80þ macrophages, matrix metalloproteinase 9 (MMP-9), inflammatory cytokines and chemokines (IL-1b, IL-6, TNF-a, CCL-2, CCL5 and CX3CL1/CX3CR1) as well as p65 NF-jB activation. Hematuria was negatively correlated with anti inflammatory IL-10 mRNA expression, Factor H levels and collagen IV content. Notably, SP infection induced expression of the tubular injury markers N-GAL andKIM-1. Increased peripheral neutrophils levels were observed in the SP-infected a1KICD89tg mice. Mechanistically, anti-Ly6G-mediated neutrophil depletion reduced SP-mediated hematuria, proteinuria and albuminuria, prevented loss of synaptopodin and nephrin, decreased renal inflammation and MMP-9 expression in a1KICD89tg mice.CONCLUSION: In a humanized mouse model of IgAN, hematuria bouts following respiratory tract infections are caused by a neutrophil-mediated alteration of the glomerular filtration barrier (podocyte damage, complement deposits and loss of Collagen IV). These findings may help to unveil novel potential therapeutic approaches to combat one of the key elements in the progression of IgAN and related conditions.Peer reviewe

Measurement of forward charged hadron flow harmonics in peripheral PbPb collisions at √sNN = 5.02 TeV with the LHCb detector

Flow harmonic coefficients, v n , which are the key to studying the hydrodynamics of the quark-gluon plasma (QGP) created in heavy-ion collisions, have been measured in various collision systems and kinematic regions and using various particle species. The study of flow harmonics in a wide pseudorapidity range is particularly valuable to understand the temperature dependence of the shear viscosity to entropy density ratio of the QGP. This paper presents the first LHCb results of the second- and the third-order flow harmonic coefficients of charged hadrons as a function of transverse momentum in the forward region, corresponding to pseudorapidities between 2.0 and 4.9, using the data collected from PbPb collisions in 2018 at a center-of-mass energy of 5.02 TeV . The coefficients measured using the two-particle angular correlation analysis method are smaller than the central-pseudorapidity measurements at ALICE and ATLAS from the same collision system but share similar features

Prototyping the DOPTEST Framework for Simulation-Based Testing of System Integration Strategies in Districts

This paper introduces the District Optimization Testing (DOPTEST) concept, which naturally extends from the Building Optimization Testing (BOPTEST) framework, for simulation-based testing of advanced control strategies in districts. While the focus of the BOPTEST framework is on individual building control, DOPTEST is meant to assess system integration strategies at a district level. This paper lays down the design requirements and modeling methodology for district emulators in DOPTEST and shows a simulation example of its first test case prototype

Leukemia Viruses

info:eu-repo/semantics/publishe

C-type natriuretic peptide regulates blood–testis barrier dynamics in adult rat testes

In adult rat testes, the blood–testis barrier (BTB) in the seminiferous epithelium must “open” (or “disassemble”) to accommodate the migration of preleptotene spermatocytes from the basal to the adluminal compartment that occurs at stage VIII of the epithelial cycle. However, the molecule(s) and/or mechanism(s) that regulate this event are unknown. In this report, C-type natriuretic peptide (CNP) was shown to be a regulator of BTB dynamics. Although Sertoli and germ cells contributed to the pool of CNP in the seminiferous epithelium, its receptor, natriuretic peptide receptor B, resided almost exclusively in Sertoli cells. CNP also expressed stage-specifically and localized predominantly at the BTB in the seminiferous epithelium at stage VIII of the epithelial cycle. A synthetic CNP-22 peptide, when added to Sertoli cell cultures, was shown to perturb Sertoli cell tight junction in vitro, causing disappearance of BTB-associated proteins (JAM-A, occludin, N-cadherin, and β-catenin) from the cell–cell interface. This inhibitory effect of CNP on the tight junction was confirmed by transient overexpression of CNP in these cells, which was mediated, at least in part, by accelerating the internalization of BTB integral membrane proteins. To validate these in vitro findings, CNP-22 was administered to testes at a dose of 0.35 or 3.5 μg per testis, which was shown to perturb the BTB integrity In vivo when the barrier function was assessed by monitoring the diffusion of a small molecular probe across the BTB. In summary, CNP secreted by Sertoli and germ cells into the BTB microenvironment regulates BTB dynamics during spermatogenesis

Transcriptional Up-Regulation of the Cyclin D2 Gene and Acquisition of New Cyclin-Dependent Kinase Partners in Human T-Cell Leukemia Virus Type 1- Infected Cells

Human T-cell leukemia virus type 1 (HTLV-1) is the etiologic agent for adult T-cell leukemia/lymphoma (ATL) and HTLV-1-associated myelopathy/tropical spastic paraparesis. Tax1 is a 40-kDa phosphoprotein, predominantly localized in the nucleus of the host cell, which functions to transactivate both viral and cellular promoters. It seems likely that HTLV-1, through expression of the viral regulatory protein Tax1, provides some initial alteration in cell metabolism predisposing the development of ATL. Here, we demonstrate that HTLV-1 infection in T-cell lines and patient samples causes overexpression of an early G1 cyclin, cyclin D2. The transcriptional up-regulation of the cyclin D2 gene is due to activation of Tax on the cyclin D2 gene. More important, we find that overexpression of cyclin D2 is accompanied by acquisition of new partners such as cyclin- dependent kinase 2 (cdk2), cdk4, and cdk6 in infected cells. This is in contrast to uninfected T cells, where cyclin D2 associates only with cdk6. Functional effects of these cyclin-cdk complexes in infected cells are shown by hyperphosphorylation of Rb and histone H1, indicators of active progression into S phase as well as changes in cellular chromatin and transcription machinery. These studies link HTLV-1 infection with changes of cellular cyclin gene expression, hence providing clues to development of T- cell leukemia