Model-Driven Sensing-Node Selection and Power Allocation for Tracking Maneuvering Targets in Perceptive Mobile Networks

Maneuvering target tracking will be an important service of future wireless networks to assist innovative applications such as intelligent transportation. However, tracking maneuvering targets by cellular networks faces many challenges. For example, the dense network and high-speed targets make the selection of the sensing nodes (SNs), e.g., base stations, and the associated power allocation very difficult, given the stringent latency requirement of sensing applications. Existing methods have demonstrated engaging tracking performance, but with very high computational complexity. In this paper, we propose a model-driven deep learning approach for SN selection to meet the latency requirement. To this end, we first propose an iterative SN selection method by jointly exploiting the majorization-minimization (MM) framework and the alternating direction method of multipliers (ADMM). Then, we unfold the iterative algorithm as a deep neural network (DNN) and prove its convergence. The proposed model-driven method has a low computational complexity, because the number of layers is less than the number of iterations required by the original algorithm, and each layer only involves simple matrix-vector additions/multiplications. Finally, we propose an efficient power allocation method based on fixed point (FP) water filling (WF) and solve the joint SN selection and power allocation problem under the alternative optimization framework. Simulation results show that the proposed method achieves better performance than the conventional optimization-based methods with much lower computational complexity

An Experimental Study of Byzantine-Robust Aggregation Schemes in Federated Learning

Byzantine-robust federated learning aims at mitigating Byzantine failures during the federated training process, where malicious participants may upload arbitrary local updates to the central server to degrade the performance of the global model. In recent years, several robust aggregation schemes have been proposed to defend against malicious updates from Byzantine clients and improve the robustness of federated learning. These solutions were claimed to be Byzantine-robust, under certain assumptions. Other than that, new attack strategies are emerging, striving to circumvent the defense schemes. However, there is a lack of systematic comparison and empirical study thereof. In this paper, we conduct an experimental study of Byzantine-robust aggregation schemes under different attacks using two popular algorithms in federated learning, FedSGD and FedAvg . We first survey existing Byzantine attack strategies and Byzantine-robust aggregation schemes that aim to defend against Byzantine attacks. We also propose a new scheme, ClippedClustering , to enhance the robustness of a clustering-based scheme by automatically clipping the updates. Then we provide an experimental evaluation of eight aggregation schemes in the scenario of five different Byzantine attacks. Our results show that these aggregation schemes sustain relatively high accuracy in some cases but are ineffective in others. In particular, our proposed ClippedClustering successfully defends against most attacks under independent and IID local datasets. However, when the local datasets are Non-IID, the performance of all the aggregation schemes significantly decreases. With Non-IID data, some of these aggregation schemes fail even in the complete absence of Byzantine clients. We conclude that the robustness of all the aggregation schemes is limited, highlighting the need for new defense strategies, in particular for Non-IID datasets.Comment: This paper has been accepted for publication in IEEE Transactions on Big Dat

Childhood Cancer Survival in the Highly Vulnerable Population of South Texas: Persistent Challenges for Adolescents and Hispanic Ethnicity

Background: This study examines childhood cancer survival rates and prognostic factors related to survival in the majority Hispanic population of South Texas (STX), whereas most other population studies in childhood cancer survival focus on populations with relatively few Hispanics. Methods: The population-based cohort study used Texas Cancer Registry data (1995-2017) to examine survival and prognostic factors. Results: The 5-year relative survival rate for STX cancer patients diagnosed at 0–19 years was 80.3% for all races/ethnicity. Hispanics had statistically significant lower 5-year relative survival rates than non-Hispanic Whites (NHW) for male and female together diagnosed at age ≥ 5 years. When comparing survival among Hispanics and NHW for the most common cancer, acute lymphocytic leukemia (ALL), the difference was most striking in the 15-19 years age range, with 47.7% Hispanic patients surviving at 5 years compared to 78.4% of NHW counterparts. The multivariable-adjusted analysis showed that males [hazard ratio (HR): 1.13], patients diagnosed at age \u3c 1 year (HR: 1.69), at 10–14 year (HR: 1.42), or at 15–19 years (HR: 1.40), and Hispanics (HR: 1.38) had significantly increased mortality risk compared to the corresponding counterparts for all cancers. Conclusions: STX Hispanics had lower 5-year relative survival than NHW especially for ALL. Male gender, diagnosis at age \u3c 1 year or 10–19 years were also associated with decreased childhood cancer survival. Despite advances in treatment, Hispanics lag significantly behind NHW. Further cohort studies in STX are warranted to identify additional factors affecting survival and to develop interventional strategies

Structure and laminar flame speed of an ammonia/methane/air premixed flame under varying pressure and equivalence ratio

This paper presents a joint experimental and numerical study on premixed laminar ammonia/methane/air flames, aiming to characterize the flame structures and NO formation and determine the laminar flame speed under different pressure, equivalence ratio, and ammonia fraction in the fuel. The experiments were carried out in a lab-scale pressurized vessel with a Bunsen burner installed with a concentric co-flow of air. Measurements of NH and NO distributions in the flames were made using planar laser-induced fluorescence. A novel method was presented for determination of the laminar flame speed from Bunsen-burner flame measurements, which takes into account the non-uniform flow in the unburned mixture and local flame stretch. NH profiles were chosen as flame front markers. Direct numerical simulation of the flames and one-dimensional chemical kinetic modeling were performed to enhance the understanding of flame structures and evaluate three chemical kinetic mechanisms recently reported in the literature. The stoichiometric and fuel-rich flames exhibit a dual-flame structure, with an inner premixed flame and an outer diffusion flame. The two flames interact, which affects the NO emissions. The impact of the diffusion flame on the laminar flame speed of the inner premixed flame is however minor. At elevated pressures or higher ammonia/methane ratios, the emission of NO is suppressed as a result of the reduced radical mass fraction and promoted NO reduction reactions. It is found that the laminar flame speed measured in the present experiments can be captured by the investigated mechanisms, but quantitative predictions of the NO distribution require further model development

Transient CDK4/6 inhibition protects hematopoietic stem cells from chemotherapy-induced exhaustion

Conventional cytotoxic chemotherapy is highly effective in certain cancers, but causes dose-limiting damage to normal proliferating cells, especially hematopoietic stem and progenitor cells (HSPCs). Serial exposure to cytotoxics causes a long-term hematopoietic compromise (‘exhaustion’), which limits the use of chemotherapy and success of cancer therapy. Here, we show that the co-administration of G1T28 (trilaciclib), a small-molecule inhibitor of cyclin-dependent kinases 4 and 6 (CDK4/6), contemporaneously with cytotoxic chemotherapy protects murine hematopoietic stem cells (HSCs) from chemotherapy-induced exhaustion in a serial 5-fluorouracil (5FU) treatment model. Consistent with a cell intrinsic effect, we show directly preserved HSC function resulting in a more rapid recovery of peripheral blood counts, enhanced serial transplantation capacity and reduced myeloid skewing. When administered to healthy human volunteers, G1T28 demonstrated excellent in vivo pharmacology and transiently inhibited bone marrow (BM) HSPC proliferation. These findings suggest that the combination of CDK4/6 inhibitors (CDK4/6i) with cytotoxic chemotherapy should provide a means to attenuate therapy-induced BM exhaustion in patients with cancer

A Genome-Wide Association Study of Psoriasis and Psoriatic Arthritis Identifies New Disease Loci

A genome-wide association study was performed to identify genetic factors involved in susceptibility to psoriasis (PS) and psoriatic arthritis (PSA), inflammatory diseases of the skin and joints in humans. 223 PS cases (including 91 with PSA) were genotyped with 311,398 single nucleotide polymorphisms (SNPs), and results were compared with those from 519 Northern European controls. Replications were performed with an independent cohort of 577 PS cases and 737 controls from the U.S., and 576 PSA patients and 480 controls from the U.K.. Strongest associations were with the class I region of the major histocompatibility complex (MHC). The most highly associated SNP was rs10484554, which lies 34.7 kb upstream from HLA-C (P = 7.8×10−11, GWA scan; P = 1.8×10−30, replication; P = 1.8×10−39, combined; U.K. PSA: P = 6.9×10−11). However, rs2395029 encoding the G2V polymorphism within the class I gene HCP5 (combined P = 2.13×10−26 in U.S. cases) yielded the highest ORs with both PS and PSA (4.1 and 3.2 respectively). This variant is associated with low viral set point following HIV infection and its effect is independent of rs10484554. We replicated the previously reported association with interleukin 23 receptor and interleukin 12B (IL12B) polymorphisms in PS and PSA cohorts (IL23R: rs11209026, U.S. PS, P = 1.4×10−4; U.K. PSA: P = 8.0×10−4; IL12B:rs6887695, U.S. PS, P = 5×10−5 and U.K. PSA, P = 1.3×10−3) and detected an independent association in the IL23R region with a SNP 4 kb upstream from IL12RB2 (P = 0.001). Novel associations replicated in the U.S. PS cohort included the region harboring lipoma HMGIC fusion partner (LHFP) and conserved oligomeric golgi complex component 6 (COG6) genes on chromosome 13q13 (combined P = 2×10−6 for rs7993214; OR = 0.71), the late cornified envelope gene cluster (LCE) from the Epidermal Differentiation Complex (PSORS4) (combined P = 6.2×10−5 for rs6701216; OR 1.45) and a region of LD at 15q21 (combined P = 2.9×10−5 for rs3803369; OR = 1.43). This region is of interest because it harbors ubiquitin-specific protease-8 whose processed pseudogene lies upstream from HLA-C. This region of 15q21 also harbors the gene for SPPL2A (signal peptide peptidase like 2a) which activates tumor necrosis factor alpha by cleavage, triggering the expression of IL12 in human dendritic cells. We also identified a novel PSA (and potentially PS) locus on chromosome 4q27. This region harbors the interleukin 2 (IL2) and interleukin 21 (IL21) genes and was recently shown to be associated with four autoimmune diseases (Celiac disease, Type 1 diabetes, Grave's disease and Rheumatoid Arthritis)

CRL4 antagonizes SCFFbxo7-mediated turnover of cereblon and BK channel to regulate learning and memory

Intellectual disability (ID), one of the most common human developmental disorders, can be caused by genetic mutations in Cullin 4B (Cul4B) and cereblon (CRBN). CRBN is a substrate receptor for the Cul4A/B-DDB1 ubiquitin ligase (CRL4) and can target voltage- and calcium-activated BK channel for ER retention. Here we report that ID-associated CRL4CRBNmutations abolish the interaction of the BK channel with CRL4, and redirect the BK channel to the SCFFbxo7ubiquitin ligase for proteasomal degradation. Glioma cell lines harbouring CRBN mutations record density-dependent decrease of BK currents, which can be restored by blocking Cullin ubiquitin ligase activity. Importantly, mice with neuron-specific deletion of DDB1 or CRBN express reduced BK protein levels in the brain, and exhibit similar impairment in learning and memory, a deficit that can be partially rescued by activating the BK channel. Our results reveal a competitive targeting of the BK channel by two ubiquitin ligases to achieve exquisite control of its stability, and support changes in neuronal excitability as a common pathogenic mechanism underlying CRL4CRBN–associated ID

Differential Gene Expression by RamA in Ciprofloxacin-Resistant Salmonella Typhimurium

Overexpression of ramA has been implicated in resistance to multiple drugs in several enterobacterial pathogens. In the present study, Salmonella Typhimurium strain LTL with constitutive expression of ramA was compared to its ramA-deletion mutant by employing both DNA microarrays and phenotype microarrays (PM). The mutant strain with the disruption of ramA showed differential expression of at least 33 genes involved in 11 functional groups. The study confirmed at the transcriptional level that the constitutive expression of ramA was directly associated with increased expression of multidrug efflux pump AcrAB-TolC and decreased expression of porin protein OmpF, thereby conferring multiple drug resistance phenotype. Compared to the parent strain constitutively expressing ramA, the ramA mutant had increased susceptibility to over 70 antimicrobials and toxic compounds. The PM analysis also uncovered that the ramA mutant was better in utilization of 10 carbon sources and 5 phosphorus sources. This study suggested that the constitutive expression of ramA locus regulate not only multidrug efflux pump and accessory genes but also genes involved in carbon metabolic pathways