Evaluating Fuel Consumption for Continuous Descent Approach Based on QAR Data

Fuel savings are a significant aspect for evaluating the current and future technologies of civil aviation. Continuous-Descent Approach (CDA), as a representative of new concepts, requires a method for evaluating its fuel benefits. However, because of unavailability of the practical operational data, it is difficult to validate whether the previous fuel consumption mechanisms are suitable. This paper presents a unique method for quantifying potential fuel benefits. This permits an easy evaluation for the new procedures without modelling before implementing field tests. The proposed method is detailed in this paper. It derives from the inherent mechanical characteristic of aircraft engine, and utilizes historical flight data, rather than modelling, to predict fuel flow rates by matching flight conditions from Quick Access Recorder (QAR) data. The result has been shown to predict fuel consumption for conventional descent with the deviation of ±0.73%. To validate such method, a case study for our designed CDA procedure is presented. Fuel consumptions in baseline scenarios are estimated to analyse the variable impacts on fuel consumption. The estimated fuel benefits are consistent with the results in the previous field tests. This analysis helps support Air Traffic Management decisions on eventual field test by reducing the validation time and cost.</p

Myricetin promotes peripheral nerve regeneration in rat model of sciatic nerve injury via regulation of BDNFAkt/ GSK-3β/mTOR signalling pathway

Purpose: To investigate the effects of myricetin on peripheral nerve regeneration in sciatic nerve crush injury model.Methods: Separate groups of rats were administered myricetin at 25, 50 or 100 mg/kg body weight/day for 2 weeks. Functional recovery following sciatic nerve injury was assessed by foot position and walking track analyses, measurement of mechanical hyperalgesia, and withdrawal reflex latency (WRL).Results: Myricetin treatment resulted in significantly enhanced recovery of sensorimotor functions as evidenced by increased scores in functional analysis tests. Myricetin treatment remarkably elevated brain derived neurotrophic factor (BDNF) expression, and also enhanced activation of Akt and mTORc1, reflecting up-regulation of PI3K/Akt/mTORC1 signalling involved in nerve regeneration.Conclusion: Myricetin enhances functional recovery and nerve regeneration in rats. These findings suggest that myricetin is a potent neuroprotective agent with potential for the management of peripheral nerve injury.Keywords: Glycogen synthase kinase 3β, Mammalian target of rapamycin (mTOR), Myricetin, Nerve regeneratio

Understanding MMPI-2 response structure between schizophrenia and healthy individuals

BackgroundUsing Minnesota Multiphasic Personality Inventory-2 (MMPI-2) clinical scales to evaluate clinical symptoms in schizophrenia is a well-studied topic. Nonetheless, research focuses less on how these clinical scales interact with each other.AimsInvestigates the network structure and interaction of the MMPI-2 clinical scales between healthy individuals and patients with schizophrenia through the Bayesian network.MethodData was collected from Wuhan Psychiatric Hospital from March 2008 to May 2018. A total of 714 patients with schizophrenia and 714 healthy subjects were identified through propensity score matching according to the criteria of the International Classification of Diseases (ICD-11). Separated MMPI-2 clinical scales Bayesian networks were built for healthy subjects and patients with schizophrenia, respectively.ResultsThe Bayesian network showed that the lower 7 scale was a consequence of the correlation between the lower 2 scale and the greater 8 scale. A solely lower 7 scale does yield neither a lower 2 scale nor a higher 8 scale. The proposed method showed 72% of accuracy with 78% area under the ROC curve (AUC), similar to the previous studies.LimitationsThe proposed method simplified the continuous Bayesian network to predict binary outcomes, including other categorical data is not explored. Besides, the participants might only represent an endemic as they come from a single hospital.ConclusionThis study identified MMPI-2 clinical scales correlation and built separated Bayesian networks to investigate the difference between patients with schizophrenia and healthy people. These differences may contribute to a better understanding of the clinical symptoms of schizophrenia and provide medical professionals with new perspectives for diagnosis

I2^2-SDF: Intrinsic Indoor Scene Reconstruction and Editing via Raytracing in Neural SDFs

In this work, we present I$^2$-SDF, a new method for intrinsic indoor scene reconstruction and editing using differentiable Monte Carlo raytracing on neural signed distance fields (SDFs). Our holistic neural SDF-based framework jointly recovers the underlying shapes, incident radiance and materials from multi-view images. We introduce a novel bubble loss for fine-grained small objects and error-guided adaptive sampling scheme to largely improve the reconstruction quality on large-scale indoor scenes. Further, we propose to decompose the neural radiance field into spatially-varying material of the scene as a neural field through surface-based, differentiable Monte Carlo raytracing and emitter semantic segmentations, which enables physically based and photorealistic scene relighting and editing applications. Through a number of qualitative and quantitative experiments, we demonstrate the superior quality of our method on indoor scene reconstruction, novel view synthesis, and scene editing compared to state-of-the-art baselines.Comment: Accepted by CVPR 202

ATP6L promotes metastasis of colorectal cancer by inducing epithelial-mesenchymal transition

ATP6L, the C subunit of the V-ATPase V0 domain, is involved in regulating the acidic tumor micro-environment and may promote tumor progression. However, the expression and functional role of ATP6L in tumors have not yet been well explored. In this study, we found that ATP6L protein overexpression was related to colorectal cancer histological differentiation (P <0.001), presence of metastasis (P <0.001) and recurrence (P = 0.02). ATP6L expression in the liver metastatic foci was higher than in the primary foci (P = 0.04). ATP6L expression was notably concomitant with epithelial-mesenchymal transition (EMT) immunohistochemical features, such as reduced expression of the epithelial marker E-cadherin (P = 0.021) and increased expression of the mesenchymal marker vimentin (P = 0.004). Results of in vitro and in vivo experiments showed that ATP6L expression could alter cell morphology, regulate EMT-associated protein expression, and enhance migration and invasion. The effect of ATP6L on metastasis was further demonstrated in a tail vein injection mice model. In addition, the mouse xenograft model showed that ATP6L-overexpressing HCT116 cells grew into larger tumor masses, showed less necrosis and formed more micro-vessels than the control cells. Taken together, our results suggest that ATP6L promotes metastasis of colorectal cancer by inducing EMT and angiogenesis, and is a potential target for tumor therapy

SIRT5 promotes IDH2 desuccinylation and G6PD deglutarylation to enhance cellular antioxidant defense

Abstract Excess in mitochondrial reactive oxygen species (ROS) is considered as a major cause of cellular oxidative stress. NADPH, the main intracellular reductant, has a key role in keeping glutathione in its reduced form GSH, which scavenges ROS and thus protects the cell from oxidative damage. Here, we report that SIRT5 desuccinylates and deglutarylates isocitrate dehydrogenase 2 (IDH2) and glucose‐6‐phosphate dehydrogenase (G6PD), respectively, and thus activates both NADPH‐producing enzymes. Moreover, we show that knockdown or knockout of SIRT5 leads to high levels of cellular ROS. SIRT5 inactivation leads to the inhibition of IDH2 and G6PD, thereby decreasing NADPH production, lowering GSH, impairing the ability to scavenge ROS, and increasing cellular susceptibility to oxidative stress. Our study uncovers a SIRT5‐dependent mechanism that regulates cellular NADPH homeostasis and redox potential by promoting IDH2 desuccinylation and G6PD deglutarylation

Original Article Hyperbaric spinal anesthesia with ropivacaine coadministered with sufentanil for cesarean delivery: a dose-response study

Abstract: Adjuvant sufentanil could achieve effective spinal anesthesia with low dose of hyperbaric ropivacaine for cesarean delivery. Two previous studies had calculated the 50% effective dose (ED50) of intrathecal ropivacaine coadministered with sufentanil for cesarean delivery. However, the 95% effective dose (ED95) of intrathecal hyperbaric ropivacaine coadministered with sufentanil for cesarean delivery remains uncertain. This study determined the ED95 of intrathecal hyperbaric ropivacaine coadministered with sufentanil for cesarean delivery. 80 ASA physical status I or II parturients undergoing elective cesarean delivery were enrolled in this prospective, randomized, double-blind investigation. A combined spinal and epidural anesthesia was performed at the L3-L4 interspace. Patients received a dose of spinal ropivacaine coadministered with sufentanil 5 μg diluted to 3.0 ml with normal saline and 0.5 ml of 10% dextrose: 7.5 mg (n = 20), 9.0 mg (n = 20), 10.5 mg (n = 20), or 12 mg (n = 20). An effective dose was defined as a dose that provided bilateral sensory block to T7 within 10 min after intrathecal drug administration and required no epidural top-up for surgery to be completed. The ED50 and ED95 values for successful anesthesia were determined using a logistic regression model. The ED50 (95% confidence interval [CI]) for successful anesthesia was 8.4 (4.0-9.8) mg and the ED95 (95% CI) was 11.4 (9.7-13.9) mg. The results show that the ED95 of intrathecal hyperbaric ropivacaine coadministered with sufentanil 5 μg for cesarean delivery was 11.4 mg. The addition of sufentanil could significantly reduce the dosage of ropivacaine

92-Gene Molecular Profiling in Identification of Cancer Origin: A Retrospective Study in Chinese Population and Performance within Different Subgroups

BACKGROUND: After cancer diagnosis, therapy for the patient is largely dependent on the tumor origin, especially when a metastatic tumor is being treated. However, cases such as untypical metastasis, poorly differentiated tumors or even a limited number of tumor cells may lead to challenges in identifying the origin. Moreover, approximately 3% to 5% of total solid tumor patients will not have to have their tumor origin identified in their lifetime. The THEROS CancerTYPE ID® is designed for identifying the tumor origin with an objective, rapid and standardized procedure. METHODOLOGY AND PRINCIPAL FINDINGS: This is a blinded retrospective study to evaluate performance of the THEROS CancerTYPE ID® in a Chinese population. In total, 184 formalin-fixed paraffin-embedded (FFPE) samples of 23 tumor origins were collected from the tissue bank of Fudan University Shanghai Cancer Center (FDUSCC). A standard tumor cell enrichment process was used, and the prediction results were compared with reference diagnosis, which was confirmed by two experienced pathologists at FDUSCC. All of the 184 samples were successfully analyzed, and no tumor specimens were excluded because of sample quality issues. In total, 151 samples were correctly predicted. The agreement rate was 82.1%. A Pearson Chi-square test shows that there is no difference between this study and the previous evaluation test performed by bioTheranostics Inc. No statistically significant decrease was observed in either the metastasis group or tumors with high grades. CONCLUSIONS: A comparable result with previous work was obtained. Specifically, specimens with a high probability score (>0.85) have a high chance (agreement rate = 95%) of being correctly predicted. No performance difference was observed between primary and metastatic specimens, and no difference was observed among three tumor grades. The use of laser capture micro-dissection (LCM) makes the THEROS CancerTYPE ID® accessible to almost all of the cancer patients with different tumor statuses

ChIP-seq and Functional Analysis of the SOX2 Gene in Colorectal Cancers

SOX2 is anHMGbox containing transcription factor that has been implicated in various types of cancer, but its role in colorectal cancers (CRC) has not been studied. Here we show that SOX2 is overexpressed in CRC tissues compared with normal adjacent tissues using immunohistochemical staining and RT-PCR. We also observed an increased SOX2 expression in nucleus of colorectal cancer tissues (46%, 14/30 cases vs. 7%, 2/30 adjacent tissues). Furthermore, knockdown of SOX2 in SW620 colorectal cancer cells decreased their growth rates in vitro cell line, and in vivo in xenograft models. ChIP-Seq analysis of SOX2 revealed a consensus sequence of wwTGywTT. An integrated expression profiling and ChIP-seq analysis show that SOX2 is involved in the BMP signaling pathway, steroid metabolic process, histone modifications, and many receptor-mediated signaling pathways such as IGF1R and ITPR2 (Inositol 1,4,5-triphosphate receptor, type 2).MOST, Chin

SIRT3-dependent GOT2 acetylation status affects the malate-aspartate NADH shuttle activity and pancreatic tumor growth

The malate–aspartate shuttle is indispensable for the net transfer of cytosolic NADH into mitochondria to maintain a high rate of glycolysis and to support rapid tumor cell growth. The malate–aspartate shuttle is operated by two pairs of enzymes that localize to the mitochondria and cytoplasm, glutamate oxaloacetate transaminases (GOT), and malate dehydrogenases (MDH). Here, we show that mitochondrial GOT2 is acetylated and that deacetylation depends on mitochondrial SIRT3. We have identified that acetylation occurs at three lysine residues, K159, K185, and K404 (3K), and enhances the association between GOT2 and MDH2. The GOT2 acetylation at these three residues promotes the net transfer of cytosolic NADH into mitochondria and changes the mitochondrial NADH/NAD+ redox state to support ATP production. Additionally, GOT2 3K acetylation stimulates NADPH production to suppress ROS and to protect cells from oxidative damage. Moreover, GOT2 3K acetylation promotes pancreatic cell proliferation and tumor growth in vivo. Finally, we show that GOT2 K159 acetylation is increased in human pancreatic tumors, which correlates with reduced SIRT3 expression. Our study uncovers a previously unknown mechanism by which GOT2 acetylation stimulates the malate–aspartate NADH shuttle activity and oxidative protection