A Probe Placement Method for Efficient Electromagnetic Attacks

Electromagnetic (EM) emissions have been explored as an effective means for non-invasive side-channel attacks. The leaked EM field from the memory bus when the data is loaded from the on-chip memory has received considerable attention in literature. Meanwhile, off-chip memory buses gradually become the new attack target due to the relative ease of access in the modern system in package technologies, such as 2.5-D integration where processing and memory chips are integrated, for example, on a silicon interposer. This paper, therefore, investigates EM snooping attacks on interposer-based off-chip memory buses. A gradient-search algorithm is proposed to locate fast (i.e. O(N)) the most efficient attack point. The effectiveness of the search algorithm and attack efficiency is evaluated on a 64-bit bus. It is demonstrated that at the optimal attack point, EM attacks can succeed with more than 10x fewer traces, compared to placing the probe to sub-optimal locations

Rare earth ion-doped Y2.95R0.05MgAl3SiO12 (R = Yb, Y, Dy, Eu, Sm) garnet-type microwave ceramics for 5G application

In this work, Y2.95R0.05MgAl3SiO12 (R=Yb, Y, Dy, Eu, Sm) microwave single-phase dielectric ce-ramics were successfully prepared via conventional ceramic technology by doping a series of rare earth elements with different ionic radius (Yb, Y, Dy, Eu, Sm) for the first time. The effects of A site occupied by rare earth elements on the microwave dielectric properties of Y2.95R0.05MgAl3SiO12 were studied by crystal structure refinement, scanning electron microscope (SEM), bond valence theory, P-V-L theory and infrared reflection spectroscopy. It was found that the ionicity of Y-O bond, the lattice energy, the bond energy and bond valance of Al(Tet)-O bond had important effects on microwave dielectric properties. Particularly, the optimum microwave dielectric properties were obtained for Y2.95Dy0.05MgAl3SiO12 sintered at 1575 °C for 6 h, with εr = 9.68, Q×f = 68,866 GHz, and τf = -35.8 ppm/°C, displaying its potential prospect in the 5G communication

Valorisation of microalgae residues after lipid extraction: Pyrolysis characteristics for biofuel production

As a promising source of renewable energy, biofuel from microalgae pyrolysis is seen as a competitive alternative to fossil fuels. However, currently, the widely applied pre-treatment process of lipid extraction results in large amounts of microalgae residues, which though with energy potential, being considered as process wastes and ignored of its re-utilization potential. In this study, a new workflow of biofuel generation from microalgae biomass through lipid extraction and pyrolysis of defatted microalgae residues was proposed and assessed. The effects of lipid extraction and pyrolysis temperature (350–750 ℃) on pyrolysis products were investigated, and pyrolysis pathways were postulated. To address the twin goals of lowering emission of pollutants and elevating energy products, an optimal pyrolysis temperature of 650 ℃ was suggested. After extraction of lipids, the relative contents of valuable products (aromatic, aliphatic hydrocarbons and fatty acids) and some harmful by-products, e.g., PAHs, significantly reduced, while other harmful substrates, e.g., nitrogen-compounds increased. Mechanistic investigations indicated that pyrolysis of proteins without the presence of lipids could promote higher production of nitrogen-containing organics and aromatics. These results reveal the effects of lipid extraction and variation of temperature on microalgal pyrolysis, and also provide a basis for full utilization of microalgae as an aid to alleviate many fossil energy problems

Establishment of noncycloplegic methods for screening myopia and pre-myopia in preschool children

PurposePre-myopia, a non-myopic refractive state, is a key concern for myopia prevention because of its association with a significantly higher risk of myopia in children under 3 years of age. Amid the myopia pandemic, its onset at younger ages is increasing, yet research on screening methods for myopia and pre-myopia in preschool children remains limited. This study aimed to establish effective noncycloplegic screening methods for myopia and pre-myopia in preschool children.MethodsThis cross-sectional study included 16 kindergartens in Shanghai, China. Uncorrected distance visual acuity (UDVA) was recorded using a logMAR visual acuity chart. Pre- and post-cycloplegic refractions were obtained using an auto-refractor (TopconKR-800). Noncycloplegic axial length (AL) and corneal curvature radius (CR) were measured using the IOL Master-700. Logistic regression models were developed to establish accurate noncycloplegic screening methods for myopia and pre-myopia.ResultsA total of 1,308 children with a mean age of 4.3 ± 0.9 years were included; among them 640 (48.9%) were girls. The myopia prevalence rate was 2.8% (n = 36), and the prevalence of pre-myopia was 21.9% (n = 286). Pre-myopia screening (cycloplegic spherical equivalent [SE] ≤ −0.5 < SE ≤0.75 diopters [D]) using UDVA exhibited an area under the receiver operating curve (AUC) of 0.52, noncycloplegic SE had an AUC of 0.70 and AL had an AUC of 0.63. The accuracy of combining the SE and AL/CR ratio was among the best with the least number of checks used, and the AUC was 0.74 for pre-myopia screening and 0.94 for myopia screening (cycloplegic SE ≤ −0.5 D). The addition of UDVA did not further improve the accuracy.ConclusionUsing UDVA alone did not achieve good accuracy in pre-myopia or myopia screening of young children. Under non-cycloplegic conditions, the combination of AL/CR and SE demonstrated favorable results for pre-myopia and myopia screening of preschool children

The association between Toll-like receptor 2 single-nucleotide polymorphisms and hepatocellular carcinoma susceptibility

<p>Abstract</p> <p>Background</p> <p>Toll-like receptors (TLR) are key innate immunity receptors participating in an immune response. Growing evidence suggests that mutations of TLR2/TLR9 gene are associated with the progress of cancers. The present study aimed to investigate the temporal relationship of single nucleotide polymorphisms (SNP) of TLR2/TLR9 and the risk of hepatocellular carcinoma (HCC).</p> <p>Methods</p> <p>In this single center-based case-control study, SNaPshot method was used to genotype sequence variants of TLR2 and TLR9 in 211 patients with HCC and 232 subjects as controls.</p> <p>Results</p> <p>Two synonymous SNPs in the exon of TLR2 were closely associated with risk of HCC. Compared with those carrying wild-type homozygous genotypes (T/T), risk of HCC decreased significantly in individuals carrying the heterozygous genotypes (C/T) of the rs3804099 (adjusted odds ratio (OR), 0.493, 95% CI 0.331 - 0.736, <it>P </it>< 0.01) and rs3804100 (adjusted OR, 0.509, 95% CI 0.342 - 0.759, <it>P </it>< 0.01). There was no significant association found in two TLR9 SNPs concerning the risk of HCC. The haplotype TT for TLR2 was associated significantly with the decreased risk of HCC (OR 0.524, 95% CI 0.394 - 0.697, <it>P </it>= 0.000). Inversely, the risk of HCC increased significantly in patients with the haplotype CC (OR 2.743, 95% CI 1.915 - 3.930, <it>P </it>= 0.000).</p> <p>Conclusions</p> <p>These results suggested that TLR2 rs3804099 C/T and rs3804100 C/T polymorphisms were closely associated with HCC. In addition, the haplotypes composed of these two TLR2 synonymous SNPs have stronger effects on the susceptibility of HCC.</p

Oncogenic state and cell identity combinatorially dictate the susceptibility of cells within glioma development hierarchy to IGF1R targeting

Glioblastoma is the most malignant cancer in the brain and currently incurable. It is urgent to identify effective targets for this lethal disease. Inhibition of such targets should suppress the growth of cancer cells and, ideally also precancerous cells for early prevention, but minimally affect their normal counterparts. Using genetic mouse models with neural stem cells (NSCs) or oligodendrocyte precursor cells (OPCs) as the cells‐of‐origin/mutation, it is shown that the susceptibility of cells within the development hierarchy of glioma to the knockout of insulin‐like growth factor I receptor (IGF1R) is determined not only by their oncogenic states, but also by their cell identities/states. Knockout of IGF1R selectively disrupts the growth of mutant and transformed, but not normal OPCs, or NSCs. The desirable outcome of IGF1R knockout on cell growth requires the mutant cells to commit to the OPC identity regardless of its development hierarchical status. At the molecular level, oncogenic mutations reprogram the cellular network of OPCs and force them to depend more on IGF1R for their growth. A new‐generation brain‐penetrable, orally available IGF1R inhibitor harnessing tumor OPCs in the brain is also developed. The findings reveal the cellular window of IGF1R targeting and establish IGF1R as an effective target for the prevention and treatment of glioblastoma

Fine-tuning of microglia polarization prevents diabetes-associated cerebral atherosclerosis

Diabetes increases the occurrence and severity of atherosclerosis. When plaques form in brain vessels, cerebral atherosclerosis causes thickness, rigidity, and unstableness of cerebral artery walls, leading to severe complications like stroke and contributing to cognitive impairment. So far, the molecular mechanism underlying cerebral atherosclerosis is not determined. Moreover, effective intervention strategies are lacking. In this study, we showed that polarization of microglia, the resident macrophage in the central nervous system, appeared to play a critical role in the pathological progression of cerebral atherosclerosis. Microglia likely underwent an M2c-like polarization in an environment long exposed to high glucose. Experimental suppression of microglia M2c polarization was achieved through transduction of microglia with an adeno-associated virus (serotype AAV-PHP.B) carrying siRNA for interleukin-10 (IL-10) under the control of a microglia-specific TMEM119 promoter, which significantly attenuated diabetes-associated cerebral atherosclerosis in a mouse model. Thus, our study suggests a novel translational strategy to prevent diabetes-associated cerebral atherosclerosis through in vivo control of microglia polarization