Federated Deep Reinforcement Learning Based Task Offloading with Power Control in Vehicular Edge Computing.

Vehicular edge computing (VEC) is a promising technology for supporting computation-intensive vehicular applications with low latency at the network edges. Vehicles offload their tasks to VEC servers (VECSs) to improve the quality of service (QoS) of the applications. However, the high density of vehicles and VECSs and the mobility of vehicles increase channel interference and deteriorate the channel condition, resulting in increased power consumption and latency. Therefore, we proposed a task offloading method with the power control considering dynamic channel interference and conditions in a vehicular environment. The objective is to maximize the throughput of a VEC system under the power constraints of a vehicle. We leverage deep reinforcement learning (DRL) to achieve superior performance in complex environments and high-dimensional inputs. However, most conventional methods adopted the multi-agent DRL approach that makes decisions using only local information, which can result in poor performance, while single-agent DRL approaches require excessive data exchanges because data needs to be concentrated in an agent. To address these challenges, we adopt a federated deep reinforcement learning (FL) method that combines centralized and distributed approaches to the deep deterministic policy gradient (DDPG) framework. The experimental results demonstrated the effectiveness and performance of the proposed method in terms of the throughput and queueing delay of vehicles in dynamic vehicular networks.

A bioisosteric approach to the discovery of novel N-aryl-N'-[4-(aryloxy)cyclohexyl]squaramide-based activators of eukaryotic initiation factor 2 alpha (eIF2α) phosphorylation.

Inhibition of translation initiation has emerging implications for the development of mechanism-based anticancer therapeutics. Phosphorylation of eIF2α is recognized as a key target that regulates the translation initiation cascade. Based on the bioisosteric replacement of urea-derived eIF2α phosphorylation activator 1, a novel series of N-aryl-N'-[4-(aryloxy)cyclohexyl]squaramide derivatives was designed and synthesized; their effects on the activation of eIF2α phosphorylation was assessed systematically. A brief structure-activity relationship analysis was established by stepwise structural optimization of the squaramide series. Subsequently, the antiproliferative activities of the selected analogues were determined in human leukemia K562 cells. We then identified 10 potent eIF2α phosphorylation activators with considerable anticancer activity. The most promising analogues 19 and 40 possessed higher cancer cell selectivity (SI = 6.16 and 4.83, respectively) than parent 1 (SI = 2.20). Finally, protein expression analysis revealed that compounds 19 and 40 induced eIF2α phosphorylation and its downstream effectors ATF4 and CHOP.

Role of Neutrophils in the Pathogenesis of Nonalcoholic Steatohepatitis.

Nonalcoholic fatty liver disease (NAFLD) includes a spectrum of liver disorders, from fatty liver to nonalcoholic steatohepatitis (NASH), cirrhosis, and hepatocellular carcinoma. Compared with fatty liver, NASH is characterized by increased liver injury and inflammation, in which liver-infiltrating immune cells, with neutrophil infiltration as a hallmark of NASH, play a critical role in promoting the progression of fatty liver to NASH. Neutrophils are the first responders to injury and infection in various tissues, establishing the first line of defense through multiple mechanisms such as phagocytosis, cytokine secretion, reactive oxygen species production, and neutrophil extracellular trap formation; however, their roles in the pathogenesis of NASH remain obscure. The current review summarizes the roles of neutrophils that facilitate the progression of fatty liver to NASH and their involvement in inflammation resolution during NASH pathogenesis. The notion that neutrophils are potential therapeutic targets for the treatment of NASH is also discussed.

Radiological Risk Factors for Neurological Deficits After Traumatic Mid and Low Lumbar Fractures.

STUDY DESIGN: Retrospective study. OBJECTIVE: We identified radiological risk factors for neurological deficits in mid and low lumbar spinal fractures. SUMMARY OF BACKGROUND DATA: Although numerous studies have focused on radiological risk factors for neurological deficits in spinal cord injury or thoracolumbar junction area fractures, few have examined mid and low lumbar fractures at the cauda equina level. METHODS: We retrospectively reviewed 71 consecutive patients who suffered acute traumatic mid and low lumbar fractures (L2-L5) corresponding to the cauda equina level, as confirmed on magnetic resonance imaging. We defined a neurological deficit as present if the patient had any sensory or motor deficit in the lower extremity or autonomic system at the initial assessment. Various computed tomography parameters of canal stenosis, vertebral body compression, sagittal alignment, interpedicular distance, and presence of vertical laminar fractures were analyzed as independent risk factors to predict neurological deficits using multivariate logistic regression analyses. RESULTS: At the initial assessment, 31 patients had neurological deficits. Fracture level, AO fracture type, canal encroachment ratio, vertebral compression ratio, interpedicular distance ratio, and presence of a vertical laminar fracture were significantly associated with the presence of neurological deficits (all P < 0.05). Multivariate logistic regression identified fracture level, canal encroachment ratio (adjusted odds ratio [aOR] 1.072, 95% confidence interval [CI] 1.018-1.129), and vertebral compression ratio (aOR 0.884, 95% CI 0.788-0.992) as independent predictors of a neurological deficit. Receiver operating characteristic curve analyses revealed that only the canal encroachment ratio had good discriminatory ability (area under the curve 0.874, 95% CI 0.791-0.957), and the optimal cutoff was 47% (canal diameter 6.6 mm) with 90.3% sensitivity and 80% specificity. CONCLUSION: The canal encroachment ratio was most strongly associated with neurological deficits in traumatic mid and low lumbar fractures, with an optimal cutoff of 47%. LEVEL OF EVIDENCE: 4.

Determination of urinary Myo-/chiro-inositol ratios from Korean diabetes patients.

Of two major forms (myo- and chiro-inositol) of inositols, only chiro-inositol enhances the activity of proteins involved in intracellular glucose metabolism. This study aims to determine the urinary myo-/chiro-inositol ratio in type 1 and type 2 diabetes patients and compare its ratio with the normal control group. The 24-hour urinary myo- and chiro-inositols in 71 Korean diabetes patients and 39 control subjects have been quantified using high-performance liquid chromatography, and their ratios have been evaluated as indices of insulin resistance. The level of 24-hour urinary myo-inositol was significantly higher in both type 1 and type 2 diabetes than with the control group, whereas the urinary chiro-inositol in type 1 or type 2 diabetes was lower than that in normal subjects. The myo-/chiro-inositol ratio in diabetes patients was higher than that in the control group. Twenty four-hour urinary myo-/ chiro-inositol ratios were significantly elevated in type 1 and type 2 diabetes patients compared to the control group, suggesting that a high ratio of urinary myo-/chiro- inositol in type 2 diabetes patients might be used for an index of insulin resistance.