Switch between critical percolation modes in city traffic dynamics

Percolation transition is widely observed in networks ranging from biology to engineering. While much attention has been paid to network topologies, studies rarely focus on critical percolation phenomena driven by network dynamics. Using extensive real data, we study the critical percolation properties in city traffic dynamics. Our results suggest that two modes of different critical percolation behaviors are switching in the same network topology under different traffic dynamics. One mode of city traffic (during nonrush hours or days off) has similar critical percolation characteristics as small world networks, while the other mode (during rush hours on working days) tends to behave as a 2D lattice. This switching behavior can be understood by the fact that the high-speed urban roads during nonrush hours or days off (that are congested during rush hours) represent effective long-range connections, like in small world networks. Our results might be useful for understanding and improving traffic resilience.Comment: 8 pages, 4 figures, Daqing Li, Ziyou Gao and H. Eugene Stanley are the corresponding authors ([email protected], [email protected], [email protected]

Attribute-based encryption for cloud computing access control: A survey

National Research Foundation (NRF) Singapore; AXA Research Fun

Identifying the most influential roads based on traffic correlation networks

Prediction of traffic congestion is one of the core issues in the realization of smart traffic. Accurate prediction depends on understanding of interactions and correlations between different city locations. While many methods merely consider the spatio-temporal correlation between two locations, here we propose a new approach of capturing the correlation network in a city based on realtime traffic data. We use the weighted degree and the impact distance as the two major measures to identify the most influential locations. A road segment with larger weighted degree or larger impact distance suggests that its traffic flow can strongly influence neighboring road sections driven by the congestion propagation. Using these indices, we find that the statistical properties of the identified correlation network is stable in different time periods during a day, including morning rush hours, evening rush hours, and the afternoon normal time respectively. Our work provides a new framework for assessing interactions between different local traffic flows. The captured correlation network between different locations might facilitate future studies on predicting and controlling the traffic flows. © 2019, The Author(s)

SIMC 2.0: Improved Secure ML Inference Against Malicious Clients

In this paper, we study the problem of secure ML inference against a malicious client and a semi-trusted server such that the client only learns the inference output while the server learns nothing. This problem is first formulated by Lehmkuhl \textit{et al.} with a solution (MUSE, Usenix Security'21), whose performance is then substantially improved by Chandran et al.'s work (SIMC, USENIX Security'22). However, there still exists a nontrivial gap in these efforts towards practicality, giving the challenges of overhead reduction and secure inference acceleration in an all-round way. We propose SIMC 2.0, which complies with the underlying structure of SIMC, but significantly optimizes both the linear and non-linear layers of the model. Specifically, (1) we design a new coding method for homomorphic parallel computation between matrices and vectors. It is custom-built through the insight into the complementarity between cryptographic primitives in SIMC. As a result, it can minimize the number of rotation operations incurred in the calculation process, which is very computationally expensive compared to other homomorphic operations e.g., addition, multiplication). (2) We reduce the size of the garbled circuit (GC) (used to calculate nonlinear activation functions, e.g., ReLU) in SIMC by about two thirds. Then, we design an alternative lightweight protocol to perform tasks that are originally allocated to the expensive GCs. Compared with SIMC, our experiments show that SIMC 2.0 achieves a significant speedup by up to $17.4\times$ for linear layer computation, and at least $1.3\times$ reduction of both the computation and communication overheads in the implementation of non-linear layers under different data dimensions. Meanwhile, SIMC 2.0 demonstrates an encouraging runtime boost by $2.3\sim 4.3\times$ over SIMC on different state-of-the-art ML models

Case Report: A Clinical and Genetic Analysis of Childhood Growth Hormone Deficiency With Familial Hypercholesterolemia

BackgroundGrowth hormone deficiency (GHD) is a developmental disorder in children characterized by low growth hormone (GH), short stature and unfavorable lipid profiles. Familial hypercholesteremia (FH) is an inborn disorder of low-density lipoprotein cholesterol (LDL-C) metabolism which results in premature cardiovascular events. The co-occurrence of GHD and FH, which may aggravate the hypercholesteremic condition in the affected individuals, had rarely been discussed in previous publication.MethodsThis work reports two cases of GHD with FH, and explores the lipid profiles of GHD children and their therapeutic response to recombinant human growth hormone (rhGH). The diagnosis of GHD is based on low peak GH level (<7 ng/mL) in GH provocation test. FH is diagnosed by high LDL-C level (≥ 4 mmol/L) and confirmed genetic mutations in the LDL-C metabolic pathway. We also searched all previously published metabolic studies on GHD children as of December 31, 2020. Information on their LDL-C, duration and dose of rhGH treatment were retrieved and summarized.ResultsThe first case was a 5.3 year-old boy. His height was 103.6 cm (SDS = -2.29) and his peak GH in provocative test was 6.37 ng/mL. Additionally, his LDL-C was 4.80 mmol/L and he harbored a heterozygous mutation for the apolipoprotein B (APOB) gene (c.10579 C > T). The second case was a 9-year-old girl at the height of 117.3 cm (SDS = -2.91). Her GH peaked at 4.99 ng/mL in insulin-induced hypoglycemic test and 2.80 ng/mL in L-dopa test. Her LDL-C was 6.16 mmol/L, and she carried a mutated copy of the low-density lipoprotein receptor (LDLR) gene (c.809 G > A). Literature review indicated that GHD children suffered from higher baseline LDL-C, but it was significantly reduced after rhGH treatment.ConclusionsFH should be considered if a GHD child has remarkably elevated LDL-C that cannot be attributed to low GH level alone. Genetic mutations in the LDL-C metabolic pathway prevent the body from effectively metabolizing lipids, thereby resulting in early-onset hypercholesteremia and probably playing a negative role in children’s growth

Hepatic Autophagy Deficiency Compromises FXR Functionality and Causes Cholestatic Injury

Autophagy is important for hepatic homeostasis, nutrient regeneration and organelle quality control. We investigated the mechanisms by which liver injury occurred in the absence of autophagy function. We found that mice deficient in autophagy due to the lack of Atg7 or Atg5, key autophagy‐related genes, manifested intracellular cholestasis with increased levels of serum bile acids, a higher ratio of TMCA/TCA in the bile, increased hepatic bile acid load, abnormal bile canaliculi and altered expression of hepatic transporters. In determining the underlying mechanism, we found that autophagy sustained and promoted the basal and upregulated expression of Fxr in the fed and starved conditions, respectively. Consequently, expression of Fxr and its downstream genes, particularly Bsep, and the binding of FXR to the promoter regions of these genes, were suppressed in autophagy‐deficient livers. In addition, co‐deletion of Nrf2 in autophagy deficiency status reversed the FXR suppression. Furthermore, the cholestatic injury of autophagy‐deficient livers was reversed by enhancement of FXR activity or expression, or by Nrf2 deletion

Separation and purification of amygdalin from thinned bayberry kernels by macroporous adsorption resins

To utilize the low-value thinned bayberry (Myrica rubra Sieb. et Zucc) kernels (TBKs) waste, an efficient method using macroporous adsorption resins (MARs) for separation and purification of amygdalin from TBKs crude extracts was developed. An aqueous crude sample was prepared from a methanol TBK extract, followed by resin separation. A series of MARs were initially screened for adsorption/desorption of amygdalin in the extract, and D101 was selected for characterization and method development. The static adsorption data of amygdalin on D101 was best fitted to the pseudo-second-order kinetics model. The solute affinity toward D101 at 30 °C was described and the equilibrium experimental data were well-fitted to Langmuir and Freundlich isotherms. Through one cycle of dynamic adsorption/desorption, the purity of amygdalin in the extract, determined by HPLC, increased about 17-fold from 4.8% to 82.0%, with 77.9% recovery. The results suggested that D101 resin effectively separate amygdalin from TBKs

Methylglyoxal-Induced Retinal Angiogenesis in Zebrafish Embryo: A Potential Animal Model of Neovascular Retinopathy

Methylglyoxal (MG) is an intermediate of glucose metabolism and the precursor of advanced glycation end products (AGEs) found in high levels in blood or tissue of diabetic patients. MG and AGEs are thought to play a major role in the pathogenesis of diabetic retinopathy. In order to determine if zebrafish is valuable to help us understand more about retinopathy, we evaluate if MG induces abnormal vascular change and angiogenesis in zebrafish in a short incubation period. We also used an inhibitor of VEGFR (PTK787) to explore the mechanistic role of VEGF in MG-induced pathogenesis. A transgenic Tg(flk1:GFP) zebrafish line was used, and the embryos were incubated with MG solution and in combination with glucose (to mimic hyperglycemia). Retinal vascular structure visible with fluorescence signal was imaged using fluorescence microscopy. The percentage of vascular area was calculated and found elevated in the MG treatment groups than that in the control group (p<0.01) which indicated increased angiogenesis induced by MG treatment. PTK787 blocked the proangiogenic effects of MG treatment. This study suggests that MG has a potential proangiogenic effect via VEGF signaling in the retina of zebrafish embryos. Therefore, this zebrafish model may be used to study neovascular retinopathy