Data Processing Pipeline for Pointing Observations of Lunar-based Ultraviolet Telescope

We describe the data processing pipeline developed to reduce the pointing observation data of Lunar-based Ultraviolet Telescope (LUT), which belongs to the Chang'e-3 mission of the Chinese Lunar Exploration Program. The pointing observation program of LUT is dedicated to monitor variable objects in a near-ultraviolet (245-345 nm) band. LUT works in lunar daytime for sufficient power supply, so some special data processing strategies have been developed for the pipeline. The procedures of the pipeline include stray light removing, astrometry, flat fielding employing superflat technique, source extraction and cosmic rays rejection, aperture and PSF photometry, aperture correction, and catalogues archiving, etc. It has been intensively tested and works smoothly with observation data. The photometric accuracy is typically ~0.02 mag for LUT 10 mag stars (30 s exposure), with errors come from background noises, residuals of stray light removing, and flat fielding related errors. The accuracy degrades to be ~0.2 mag for stars of 13.5 mag which is the 5{\sigma} detection limit of LUT.Comment: 10 pages, 7 figures, 4 tables. Minor changes and some expounding words added. Version accepted for publication in Astrophysics and Space Science (Ap&SS

Prediction of lymph node metastasis in rectal cancer: comparison between shear-wave elastography based ultrasomics and MRI

PURPOSEWe aimed to explore the diagnostic efficiency of shear-wave elastography (SWE) ultrasomics in the preoperative prediction of lymph node (LN) metastasis in rectal cancer.METHODSThis study included 87 patients with pathologically confirmed rectal cancer, with data gathered from August 2017 to August 2018. A total of 1044 ultrasomics features of rectal tumor were collected with AK software from the SWE examinations. The least absolute shrinkage and selection operator (LASSO) regression model was used for feature selection and building a SWE ultrasomics signature. The diagnostic performance was evaluated with an area under the receiver operating characteristic curve (AUC) analysis. Then, the diagnostic performance of the SWE ultrasomics signature was compared with magnetic resonance imaging (MRI).RESULTSOf the 87 patients, 40 (46.0%) had LN metastasis. Thirteen ultrasomics features of rectal tumor were selected as the most significant features. The SWE ultrasomics signature correlated with LN metastasis (p < 0.001). Patients with LN metastasis had higher signature than patients without LN metastasis. In terms of diagnostic performance, SWE ultrasomics signature was significantly superior to MRI (AUC, 0.883 vs. 0.760, p = 0.034). The diagnostic accuracy, sensitivity, specificity, positive predictive value (PPV), and negative predictive value (NPV) of SWE ultrasomics signature were 82.8%, 87.5%, 78.8%, 77.8%, and 88.1%, respectively, while those of MRI were 75.9%, 77.5%, 74.5%, 72.1%, and 79.6%, respectively.CONCLUSIONSWE ultrasomics is a more accurate predictive method for identifying LN metastasis preoperatively than MRI. Thus, SWE ultrasomics might be used to better guide preoperative individual therapies for patients with rectal cancer

Effects of high glucose on expression of OPG and RANKL in rat aortic vascular smooth muscle cells

AbstractObjectiveTo explore effect of high glucose on expression of osteoprotegerin (OPG) and receptor activator of NF– κ B ligand (RANKE) in rat aortic vascular smooth muscle cells.MethodsSD rats were intraperitoneally injected with streptozotocin, OPG and RANKL expression in rat thoracic aortas were detected by immunohistochemical staining. In cultured vascular smooth muscle cells (VSMCs) (A7r5), qRT–PCR and Western blot analysis were used to examine the mRNA and protein levels of OPG and RANKL.ResultsOur results demonstrated that OPG expression was increased in hyperglycemic rat aortic VSMCs, while RANKL expression was decreased. Besides, in vitro experiments high glucose induced OPG expression, but depressed RANKL expression by dose– and time–dependent manner in cultured A7r5.ConclusionsOur findings suggested that high glucose could promote the expression of OPG, and inhibit the expression of RANKL in VSMCs, which may be partly be the molecular mechanism of diabetic vascular calcification

Exploring the common pathogenesis of Alzheimer’s disease and type 2 diabetes mellitus via microarray data analysis

BackgroundAlzheimer’s Disease (AD) and Type 2 Diabetes Mellitus (DM) have an increased incidence in modern society. Although more and more evidence has supported that DM is prone to AD, the interrelational mechanisms remain fully elucidated.PurposeThe primary purpose of this study is to explore the shared pathophysiological mechanisms of AD and DM.MethodsDownload the expression matrix of AD and DM from the Gene Expression Omnibus (GEO) database with sequence numbers GSE97760 and GSE95849, respectively. The common differentially expressed genes (DEGs) were identified by limma package analysis. Then we analyzed the six kinds of module analysis: gene functional annotation, protein–protein interaction (PPI) network, potential drug screening, immune cell infiltration, hub genes identification and validation, and prediction of transcription factors (TFs).ResultsThe subsequent analyses included 339 common DEGs, and the importance of immunity, hormone, cytokines, neurotransmitters, and insulin in these diseases was underscored by functional analysis. In addition, serotonergic synapse, ovarian steroidogenesis, estrogen signaling pathway, and regulation of lipolysis are closely related to both. DEGs were input into the CMap database to screen small molecule compounds with the potential to reverse AD and DM pathological functions. L-690488, exemestane, and BMS-345541 ranked top three among the screened small molecule compounds. Finally, 10 essential hub genes were identified using cytoHubba, including PTGS2, RAB10, LRRK2, SOS1, EEA1, NF1, RAB14, ADCY5, RAPGEF3, and PRKACG. For the characteristic Aβ and Tau pathology of AD, RAPGEF3 was associated significantly positively with AD and NF1 significantly negatively with AD. In addition, we also found ADCY5 and NF1 significant correlations with DM phenotypes. Other datasets verified that NF1, RAB14, ADCY5, and RAPGEF3 could be used as key markers of DM complicated with AD. Meanwhile, the immune cell infiltration score reflects the different cellular immune microenvironments of the two diseases.ConclusionThe common pathogenesis of AD and DM was revealed in our research. These common pathways and hub genes directions for further exploration of the pathogenesis or treatment of these two diseases

Sub-rapid solidification microstructure characteristics and control mechanisms of twin-roll cast aluminum alloys: A review

Rapid growth in industrial sectors such as automotive and shipbuilding has highlighted the significance of strip casting technology to produce lightweight alloys, particularly aluminum alloys widely used in both industrial production and daily life. Twin-roll casting (TRC), as an economically and environmentally friendly method for slab/strip production and processing, has attracted significant interest from researchers. However, the development of TRC aluminum alloys faces many challenges due to limited understanding of microstructural characteristics and control mechanisms. To further enhance comprehension of TRC aluminum alloys, this article reviews the influencing parameters, control methods, and existing issues related to TRC sub-rapid solidification (SRS) microstructure. It firstly summarizes TRC equipment types and their solidification characteristics, followed by a detailed analysis on key parameters affecting the evolution of TRC microstructure including rolling speed, roll separation force (RSF), and heat transfer coefficient (HTC). Finally, solutions to TRC defects are summarized and evaluated alongside their underlying mechanisms. This article provides a comprehensive review of the characteristics and control mechanisms of TRC microstructure while offering valuable insights for the future production of high-quality TRC aluminum strips

Risk Factors in Predicting Prognosis of Neonatal Bacterial Meningitis—A Systematic Review

Background: Neonatal bacterial meningitis is a severe infection with high mortality and morbidity. It is necessary to identify factors associated with a high risk of a poor prognosis so that we can prevent them with more appropriate treatments. This study was performed to summarize the prognostic factors known to predict adverse outcomes in neonatal bacterial meningitis.Methods: The Medline/PubMed, Cochrane Library and Embase databases were searched for studies of prognostic risk factors in neonates with bacterial meningitis. Studies published from the initiation of the database to April 30th, 2017 were included. The quality of cohort studies was assessed by the Newcastle-Ottawa Scale (NOS). The quality of cross-section studies was assessed by the Agency for Healthcare Research and Quality (AHRQ) scale. Each prognostic factor known to cause adverse outcomes is summarized.Results: Sixteen studies were identified, including 7 cohort studies and 9 cross section studies. Seizure and high protein levels in the cerebrospinal fluid (CSF) predict a poor prognosis in this disease. Coma, the need for ventilation support, and leukopenia also had some value for predicting poor prognoses. A bulging anterior fontanelle was valuable for predicting mortality. Low CSF glucose levels, thrombocytopenia, gestational age (GA) &lt; 37 weeks and an altered sensorium were correlated with a poor prognosis. A birth weight &lt; 2500 g, early onset meningitis and positive CSF cultures were correlated with mortality.Conclusions: This study provides a preliminary exploration of prognostic factors in neonatal bacterial meningitis and thereby fills some of the gaps in the study of prognoses in this disease. These prognostic factors can be used to predict and estimate outcomes in neonatal bacterial meningitis. Without a meta-analysis, the reliability of these factors cannot be assured. In addition, these results emphasize that there is an urgent need for a standardized protocol for follow-up and well-designed prognostic studies in neonatal bacterial meningitis

RPS23RG1 modulates tau phosphorylation and axon outgrowth through regulating p35 proteasomal degradation

Tau蛋白病（Tauopathies）是由过度磷酸化的tau蛋白聚集形成神经纤维缠结为特征的一类神经退行性疾病，包括阿尔茨海默病（Alzheimer’s disease, AD）、进行性核上性麻痹（Progressive superanuclear palsy, PSP）、额颞叶痴呆（Frontotemporal dementia, FTD）等。随着全球社会结构的老龄化，tau蛋白病患者比率迅速增加，给个人和社会带来巨大的经济及精神负担。厦门大学神经科学研究所张云武教授团队最新发现RPS23RG1（RR1）的胞内羧基端区域能够与Cdk5激酶的激活蛋白p35的氨基端相互作用，介导p35的膜定位并影响其泛素化降解，从而调控在tau蛋白异常磷酸化过程中发挥重要作用的Cdk5激酶的活性。团队研究表明RPS23RG1通过其胞内羧基端与p35相互作用，介导p35膜结合和降解，从而抑制Cdk5活性，平衡tau磷酸化水平，促进轴突生长。此外，RPS23RG1的跨膜区与腺苷酸环化酶AC相互作用，抑制GSK3-β活性，同样控制tau过度磷酸化。提示RPS23RG1是改善tau过度磷酸化水平及治疗tau蛋白病的潜在靶点。 厦门大学医学院神经科学研究所博士后赵东栋为该研究第一作者，张云武教授为通讯作者。【Abstract】Tauopathies are a group of neurodegenerative diseases characterized by hyperphosphorylation of the microtubule-binding protein, tau, and typically feature axon impairment and synaptic dysfunction. Cyclin-dependent kinase5 (Cdk5) is a major tau kinase and its activity requires p35 or p25 regulatory subunits. P35 is subjected to rapid proteasomal degradation in its membrane-bound form and is cleaved by calpain under stress to a stable p25 form, leading to aberrant Cdk5 activation and tau hyperphosphorylation. The type Ib transmembrane protein RPS23RG1 has been implicated in Alzheimer’s disease (AD). However, physiological and pathological roles for RPS23RG1 in AD and other tauopathies are largely unclear. Herein, we observed retarded axon outgrowth, elevated p35 and p25 protein levels, and increased tau phosphorylation at major Cdk5 phosphorylation sites in Rps23rg1 knockout (KO) mice. Both downregulation of p35 and the Cdk5 inhibitor roscovitine attenuated tau hyperphosphorylation and axon outgrowth impairment in Rps23rg1 KO neurons. Interestingly, interactions between the RPS23RG1 carboxyl-terminus and p35 amino-terminus promoted p35 membrane distribution and proteasomal degradation. Moreover, P301L tau transgenic (Tg) mice showed increased tau hyperphosphorylation with reduced RPS23RG1 levels and impaired axon outgrowth. Overexpression of RPS23RG1 markedly attenuated tau hyperphosphorylation and axon outgrowth defects in P301L tau Tg neurons. Our results demonstrate the involvement of RPS23RG1 in tauopathy disorders, and implicate a role for RPS23RG1 in inhibiting tau hyperphosphorylation through homeostatic p35 degradation and suppression of Cdk5 activation. Reduced RPS23RG1 levels in tauopathy trigger aberrant Cdk5-p35 activation, consequent tau hyperphosphorylation, and axon outgrowth impairment, suggesting that RPS23RG1 may be a potential therapeutic target in tauopathy disorders.This work was supported by grants from National Key Research and Development Program of China (2016YFC1305903 and 2018YFC2000400 to Y-wZ), National Natural Science Foundation of China (81771377, U1705285, 91332112, and 81225008 to Y-wZ), Fundamental Research Funds for the Central Universities (20720180049 to Y-wZ), the Fujian Provincial Health Commission-Education Department Joint Tackling Plan (WKJ2016-2-18 to F-rL), and Postdoctoral Science Foundation of China (2020M671948 to DZ)