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The features of lumbar curves in patients with lumbar spondylolisthesis (LS) are unclear. The aim of this retrospective study was to present the clinical and radiologic characteristics of scoliosis due to LS and LS concurrent with main thoracolumbar/lumbar adolescent idiopathic scoliosis (AIS).This study was conducted as a single-center retrospective comparative study on 56 pediatric spondylolisthesis patients with main thoracolumbar/lumbar curves. Cases were divided into 2 groups according to the course of scoliosis after spinal surgery of LS. Sagittal spinopelvic parameters and scoliotic characteristics were compared between the 2 groups.The prevalence of scoliosis was 15.3% in pediatric LS patients in our study population. Lumbar lordosis (LL), Cobb angle, apical rotation, and coronal deformity angular ratio (C-DAR) were higher in the LS concurrent with AIS group than in the LS with functional scoliosis group (P0.05), while curve span, apical vertebral translation, and central sacral vertical line to C7 plumb line were lower (P0.05). Logistic regression analyses and receiver operating characteristic curves showed that LL and C-DAR were significant risk factors of unresolved lumbar curves after spinal surgery for LS, with a cutoff value of 51.5°and 3.5, respectively.Lumbar scoliosis may develop due to LS, or a concurrent condition to LS. LL and C-DAR are the features that differentiate AIS from functional scoliosis in patients with LS.

Chemically pretreating lignocellulose has been widely used in the production of clean energy. An energy grass called hybrid Pennisetum was pretreated with different H2SO4 and NaOH concentrations to analyse the effects of an acid and alkali pretreatment on the degradation of hybrid Pennisetum lignocellulose. The chemical composition, hydrolyzed sugar yield, and microstructure were determined. The results showed that a NaOH pretreatment retained more cellulose and removed more lignins, while a H2SO4 pretreatment significantly inhibited the removal of lignins and increased hemicellulose degradation. X-ray diffraction analysis indicated that increasing the concentration of NaOH or H2SO4 could intensify the cellulose polymerization; this effect was stronger with NaOH compared to H2SO4. Scanning electron microscopy images showed that the cellulose bundles pretreated with H2SO4 were arranged tightly, while the cellulose bundles pretreated with NaOH were loose. Fourier transform infrared spectroscopy exhibited that the ether/ester bond between lignins and carbohydrates was broken by the H2SO4 pretreatment. The NaOH pretreatment increased the number of carbonyl and hydroxyl groups, resulting in more hydrophilic lignins, enabling greater facile degradation. Although the two methods are different in terms of destroying the structure of lignocellulose, the NaOH pretreatment can retain more cellulose, which is beneficial to subsequent ethanol production.

A semi-supervised learning based EEG signal detection method was studied in this paper. The feature engineering system of this paper was established, which contains novel AutoEncoders mapping features. The optimal channel combination for all subjects was determined to improve recognition accuracy by ReliefF algorithm and recursive feature elimination. What’s more, the semi-supervised learning method based on pseudo-labelling was introduced to the character recognition method, in which the training samples were dynamically reorganized and updated, so that the proposed method could complete the symbol recognition with limited number of training samples. Based on the features extacted and the optimal channel combination, the recognition accuracy of the character recognition method can reach up to 100%. &nbsp

Owing to the exorbitant overpotential and serious carrier recombination of graphitic carbon nitride (g-C3N4), noble metal (NM) is usually served as the H2 evolution co-catalyst. Although the NM (such as Pt) nanoparticles can reduce the H2 evolution overpotential, the weak Van der Waals interaction between Pt and g-C3N4 makes against the charge transfer. Herein, the solvothermal method is developed to achieve semi-chemical interaction between Pt and g-C3N4 nanotube (Pt-CNNT) for fast charge transfer. Moreover, the generated in-plane homojunction of CNNT can accelerate charge separation and restrain recombination. Meanwhile, the metallic Pt is an excellent H2 evolution co-catalyst. Photo/electrochemical tests verify that the semi-chemical interaction can improve photogenerated charge separation and transferability of CNNT. As a result, the photocatalytic H2 evolution turnover frequency (TOF) of Pt-CNNT under visible light irradiation reaches up to 918 h−1, which is one of the highest in the g-C3N4-based photocatalysts. This work provides a new idea to improve the charge transfer for efficient photocatalytic H2 evolution.

Backgroud: Transglutaminases (TGs) are multifunctional enzymes with transglutaminase cross-linking, atypical GTPase/ATPase and kinase activity. Here, an integrated comprehensive analysis shows the genomic, transcriptomic and immunological landscapes of the TGs varies among different cancers. Methods Gene expression pattern and immune cell infiltration in pan-cancer were obtained from The Cancer Genome Atlas (TCGA) databases and Gene Set Enrichment Analysis (GSEA) datasets. Western blotting, immunofluorescence, ELISA, and orthotopic xenograft model were performed to validate our database-derived results. Results The overall expression of TGs (designated as TG score) is significantly upregulated in multiple cancers and related to worse patient survial. The expression of the TG family can be regulated by multiple mechanisms at the genetic, epigenetic and transcriptional levels. Transcriptionfactors crucial for epithelial to mesenchymal transition (EMT) are commonly correlated with TG score in many cancer types. Importantly, TGM2 expression displays a close connection with the chemoresistances of a wide range of chemodrugs. TGM2, F13A1 and overall TG score are positively correlated with the infiltration of immune cells in all cancer types tested. Functional and clinical verification reveals that higher TGM2 expression is linked with worse patient survival, increased IC50 value of gemcitabine, and abundant tumor-infiltrating macrophages in pancreatic cancer. Mechanistically, increased C-C motif chemokine ligand 2 (CCL2) release affored by TGM2 contributes to macrophage infiltration with tumor microenvironment. Conclusions These results reveal the relevances and molecular networks of TG genes in human cancers, highlighting the significance of TGM2 in pancreatic cancer which may provide some promising directions for immunotherapy and dealing with chemoresistance.

Concrete structures in marine environments often face durability problems owing to the coupled action of external loads and chloride-ion erosion. Therefore, in this study, we conducted chloride ion tests on damaged concrete at four tensile stress levels and three varying number of load cycles. The test results indicate that an increase in the tensile stress and number of load cycles results in a gradual increase in the concrete damage coefficient. At fewer cycles, 50% tensile stress was the critical threshold point of damage; the damage was evident beyond this range. As the number of cycles increased, the damage increased gradually up to the critical threshold and thereafter increased rapidly. With an increase in the tensile stress level, the diffusion coefficient of chloride ions increased gradually; the loading degree improved the permeability of chloride ions. In addition, based on the theory of linear fatigue cumulative damage to concrete, a mathematical model of the relationship between the load factor and concrete damage coefficient was established. Using this model, a prediction model for the chloride ion diffusion coefficient was proposed considering the tensile stress level, load cycle number, and other load factors.

Nadia Quignot,1 Heng Jiang,1 Indraraj Umesh Doobaree,2 Jan Lehmann,3 Ola Ghatnekar4 1Evidence & Access, Certara France, Paris, France; 2Evidence & Access, Certara UK, Sheffield, UK; 3Department of Urology, Städtisches Krankenhaus, Kiel, Germany; 4Ferring Pharmaceuticals, Kastrup, DenmarkCorrespondence: Nadia Quignot, Certara France, 54 Rue de Londres, Paris, 75008, France, Tel +3 318 514 2683, Email nadia.quignot@certara.comBackground: Intermediate and high-risk non-muscle-invasive bladder cancer (NMIBC) is typically managed with transurethral resection of the bladder tumour (TURBT) followed by intravesical Bacillus Calmette–Guérin (BCG) immunotherapy; however, NMIBC patients can become refractory or unresponsive to BCG treatment, and/or progress to muscle-invasive bladder cancer (MIBC). Healthcare resource utilization (HCRU) and costs in these patient populations are high.Methods: A retrospective longitudinal cohort design of adult (≥ 18 years) patients with bladder cancer and BCG treatment (01/01/2012– 31/12/2017) was conducted using data from a representative subset of the German statutory health insurance database. During the follow-up period after last BCG, patients were categorized into subgroups of No further NMIBC treatment, Continuous treatment for NMIBC, or MIBC evidence; HCRU and costs were tabulated for each subgroup and for the entire cohort.Results: A total of 1049 patients met the study inclusion criteria (mean age, 70.9 years; 84.8% male). Across the different subgroups, patients showing MIBC evidence had more than two times higher hospitalization rates compared to the other subgroups. Overall, the entire BCG-treated cohort’s total direct medical cost including hospitalizations, outpatient care and drugs was € 33.9 million and € 9250 per patient-year. Cost for patients with MIBC evidence was much higher, at € 17,983 per patient-year, than patients with No further NMIBC treatment (€ 6617) and patients with Continuous treatment for NMIBC (€ 7786). Across the subgroups, hospitalization was the largest driver of cost and contributed the most to cost for those with MIBC evidence.Conclusion: The overall cost burden of this BCG-treated cohort of 1049 patients is high (€ 38 million whereof 4.1 million are indirect costs) over a mean follow-up of 3.9 years; economic burden is especially substantial for patients who fail BCG treatment and those who progress.Keywords: urinary bladder neoplasm, retrospective study, healthcare cost, intravesical instillation, healthcare resource

Tumor-associated macrophages (TAM) represent key regulators of the complex interplay between cancer and the immune microenvironment. Matricellular protein SPON2 is essential for recruiting lymphocytes and initiating immune responses. Recent studies have shown that SPON2 has complicated roles in cell migration and tumor progression. Here we report that, in the tumor microenvironment of hepatocellular carcinoma (HCC), SPON2 not only promotes infiltration of M1-like macrophages but also inhibits tumor metastasis. SPON2-α4β1 integrin signaling activated RhoA and Rac1, increased F-actin reorganization, and promoted M1-like macrophage recruitment. F-Actin accumulation also activated the Hippo pathway by suppressing LATS1 phosphorylation, promoting YAP nuclear translocation, and initiating downstream gene expression. However, SPON2-α5β1 integrin signaling inactivated RhoA and prevented F-actin assembly, thereby inhibiting HCC cell migration; the Hippo pathway was not noticeably involved in SPON2-mediated HCC cell migration. In HCC patients, SPON2 levels correlated positively with prognosis. Overall, our findings provide evidence that SPON2 is a critical factor in mediating the immune response against tumor cell growth and migration in HCC.Significance: Matricellular protein SPON2 acts as an HCC suppressor and utilizes distinct signaling events to perform dual functions in HCC microenvironment.Graphical Abstract: http://cancerres.aacrjournals.org/content/canres/78/9/2305/F1.large.jpg. Cancer Res; 78(9); 2305–17. ©2018 AACR.

Supplymentary data figure 1-8 and table 1-2

Purpose:Extensive research has reported that the tumor microenvironment components play crucial roles in tumor progression. Thus, blocking the supports of tumor microenvironment is a promising approach to prevent cancer progression. We aimed to determine whether blocking extracellular ATP–P2RY2 axis could be a potential therapeutic approach for PDAC treatment.Experimental Design:Expression of P2RY2 was determined in 264 human PDAC samples and correlated to patient survival. P2RY2 was inhibited in human PDAC cell lines by antagonist and shRNA, respectively, and cell viability, clonogenicity, and glycolysis were determined. RNA sequencing of PDAC cell line was applied to reveal underlying molecular mechanisms. Multiple PDAC mouse models were used to assess the effects of the P2RY2 inhibition on PDAC progression.Results:P2RY2 was upregulated and associated with poor prognosis in PDAC. Activated P2RY2 by increased extracellular ATP in tumor microenvironment promoted PDAC growth and glycolysis. Further studies showed that the agonist-activated P2RY2 triggered PI3K/AKT–mTOR signaling by crosstalk with PDGFR mediated by Yes1, resulting in elevated expression of c-Myc and HIF1α, which subsequently enhanced cancer cell glycolysis. Genetic and pharmacologic inhibition of P2RY2 impaired tumor cell growth in subcutaneous and orthotopic xenograft model, as well as delayed tumor progression in inflammation-driven PDAC model. In addition, synergy was observed when AR-C118925XX, the selective antagonist of P2RY2 receptor, and gemcitabine were combined, resulting in prolonged survival of xenografted PDAC mice.Conclusions:These findings reveal the roles of the P2RY2 in PDAC metabolic reprogramming, suggesting that P2RY2 might be a potential metabolic therapeutic target for PDAC.

Supplementary figures of expression of SPON2, integrin subunit, LATS1 and YAP, effect of SPON2 on M2-like TAM infiltration, co-location of SPON2 and integrin α4/α5, influence of RhoA T19N/Q63L and Rac1 T17N mutants on active RhoA and Rac1, effect of chemokines on primed THP-1 cell migration

Supplementary materials and methods of isolation of hMC, immunohistochemical and H&E staining, 3D spheroid analysis, PLA, q-PCR, lentivirus production and cell transduction, siRNA, production of rSPON2, ELISA assay and chemokine assay

1,25-Dihydroxyvitamin D3 (1,25(OH)2D3)-mediated intestinal calcium (Ca) absorption supplies Ca for proper bone mineralization during growth. We tested whether vitamin D receptor (VDR)-mediated 1,25(OH)2D3 signaling is critical for adult Ca absorption and bone by using mice with inducible Vdr gene knockout in the whole intestine (villin-CreERT2+/− × Vdrf/f, WIK) or in the large intestine (Cdx2-CreERT2+/− ×Vdrf/f, LIK). At 4-month-old, Vdr alleles were recombined (0.05 mg tamoxifen/g BW, intraperitoneally [i.p.], 5 days) and mice were fed diets with either 0.5% (adequate) or 0.2% (low) Ca. Ca absorption was examined after 2 weeks while serum 1,25(OH)2D3, bone mass, and bone microarchitecture were examined after 16 weeks. Intestinal and renal gene expression was measured at both time points (n = 12/genotype/diet/time point). On the 0.5% Ca diet, all phenotypes in WIK and LIK mice were similar to the controls. Control mice adapted to the 0.2% low-Ca diet by increasing renal Cyp27b1 mRNA (3-fold), serum 1,25(OH)2D3 level (1.9-fold), and Ca absorption in the duodenum (Dd, + 131%) and proximal colon (PCo, + 28.9%), which prevented bone loss. In WIK mice, low-Ca diet increased serum 1,25(OH)2D3 (4.4-fold) but Ca absorption remained unaltered in the Dd and PCo. Consequently, significant bone loss occurred in WIK mice (e.g., cortical thickness, Ct.Th, −33.7%). LIK mice adapted to the low-Ca diet in the Dd but not the PCo, and the effect on bone phenotypes was milder (e.g., Ct.Th, −13.1%). Our data suggest intestinal VDR in adult mice prevents bone loss under low Ca intake but is dispensable under adequate calcium intake.

Blood vessels play a role in osteogenesis and osteoporosis; however, the role of vascular metabolism is unclear. The present study found that ovariectomized mice exhibit reductions in bone blood vessel density and expression of endothelial glycolytic regulator pyruvate kinase M2 (PKM2). Additional data showed that endothelial cell (EC)-specific deletion of Pkm2 impair osteogenesis and worsen osteoporosis in mice. This was attributed to the impaired differentiation ability toward osteoblast of bone mesenchymal stem cells (BMSCs). Mechanistically, EC-specific deletion of Pkm2 reduce serum lactate levels secreted by ECs, which affect histone lactylation of BMSCs. We identified collagen type I alpha 2 chain, cartilage oligomeric matrix protein, ectonucleotide pyrophosphatase/phosphodiesterase 1, and transcription factor 7 like 2 as histone H3K18 lactylation-regulated osteogenic genes using joint CUT&Tag and RNA-sequencing analyses. The overexpression of PKM2 in ECs, addition of lactate, and exercise were observed to restore the phenotype of endothelial Pkm2-deficient mice. Furthermore, metabolomics of the serum indicated that osteoporosis patients showed a relatively low lactate level. The histone lactylation and related osteogenic genes of BMSCs in osteoporosis patients also decreased. In conclusion, the glycolysis of ECs fuels the differentiation of BMSCs into osteoblasts through histone lactylation, and exercise partially ameliorates osteoporosis through increased serum lactate.

Subarachnoid hemorrhage (SAH) is a rare complication secondary to cerebrospinal fluid (CSF) leakage during spinal surgery, but the specific cause of bleeding is still unclear. In this retrospective single-center study, we studied cases of acute SAH after spinal surgery to identify the related risk factors for bleeding.A total of 441 patients with CSF leakage who underwent spinal surgery from 2011 to 2020 were retrospectively analyzed. According to whether postoperative SAH occurred, the patients were divided into the SAH group and the control group. By comparing the demographic data, past history, imaging data, intraoperative findings, perioperative complications, and treatment conditions in the 2 groups to identify the risk factors for SAH, we aimed to provide guidance for the prevention of SAH after spinal surgery.In our study, the incidence of CSF during spinal surgery is 3.04%, and the rate for SAH associated with spine operation is 0.16%. In the SAH group, 17 patients (73.9%) had preoperative hypertension, and 3 patients (13.0%) had diabetes. The intraoperative CSF leakage was approximately 118.4 ± 56.9 mL. The mean postoperative drainage was 15.4 ± 5.8 mL/hour. Compared with the SAH group, the control group had 123 patients (29.4%) with hypertension before the operation and 40 patients (9.6%) with diabetes. The intraoperative CSF leakage was approximately 76.3 ± 23.0 mL, and the mean postoperative continuous drainage was 9.7 ± 2.1 mL/hour. Binary logistic regression analysis showed that hypertension, intraoperative CSF leakage, and postoperative CSF continuous drainage speed were related to SAH.The rapid leakage of CSF caused by rupture of the dural sac during surgery and the rapid drainage of CSF after surgery were closely related to the occurrence of SAH. In addition, hypertension was a factor related to SAH during spinal surgery.

Both forkhead box O (FOXO) and nuclear factor erythroid-derived 2-like-2 (Nrf2) are key transcription factors related to stress responses. Whereas limited studies in mammals and Caenorhabditis elegans have revealed the interaction between FoxO/DAF-16 and Nrf2/SKN-1, the role of FOXO in metabolic detoxification and regulation of the Nrf2-Keap1 signaling pathway are poorly understood in insects.Using Tribolium castaneum as a model organism, we found that RNA interference-mediated knockdown of FOXO enhanced deltamethrin-induced lethality by affecting the messenger RNA (mRNA) levels of CYP6BQ cluster genes. We further demonstrated that injection of dsFOXO into the beetle larvae decreased expression of CncC and KEAP1 at both the mRNA and protein level. Notably, dual-luciferase and electrophoretic mobility shift assays both confirmed direct regulation of CncC by FOXO, whereas Keap1 was directly regulated by CncC.FOXO can directly regulate the expression of CncC and indirectly regulate the expression of Keap1 through CncC. The data provide insights into the regulatory mechanisms of the Nrf2-Keap1 signaling pathway in insects.

Depression is a prevalent and disabling mental disorder that frequently co-occurs with a wide range of chronic conditions. Past evidence suggests that depression could be associated with the all-cause mortality and other disease mortality in Western populations, but little is known about the relationship in the Chinese population. Therefore, we investigated the associations between self-reported depression and all-cause and specific-cause mortality in Chinese adult populations.The Patient Health Questionnaire-9 (PHQ-9) was used to measure depressive symptoms among 8,151 adult participants drawn from the general population of Guizhou province, China. Participants death and cause of death were determined by linking with the official death records and certificates up to June 2021. Cause of death was coded according to ICD-10 then categorized as either cardiovascular disease (CVD, I00-I99), cancer (C00-C97) or other cause. Cox proportional hazard regression was used to examine the associations of self-reported depression with all-cause mortality and cause-specific mortality.With a median follow-up of 7.4 years, 8,151 participants (52.6% women) at baseline were included in the analysis. The multivariable cox hazard regression models showed that participants with moderate and major depression had the highest hazard ratio (HR) for risk of all-cause mortality (HR=5.65, 95% CI 3.09-10.33), CVD mortality (HR=5.66, 95% CI 2.02-15.84), and cancer mortality (HR=7.21, 95% CI 2.00-25.99), compared with participants had no or mild depression.Our findings suggested that depression was a risk factor for mortality, with greater risk for greater severity. Clinicians should be aware of the increased risk of mortality in populations with depression.

The construction of microporous organic polymers (MOPs) with sustainable building blocks is essential for their scale-up preparation and practical applications.

Aberrant DNA methylation of genes is closely linked to many aspects of tumor development. This study focuses on the effect of DNA hypermethylation of von Willebrand factor C domain containing 2 (VWC2) on colorectal cancer (CRC) progression and the underpinning mechanism. According to data in the bioinformatic systems, VWC2 had the highest degree of DNA methylation in colonic adenocarcinoma, and it showed DNA hypermethylation in rectal adenocarcinoma as well. CRC and the para-tumorous tissues were collected from 86 patients. VWC2 was expressed at low levels in CRC samples and inversely correlated with tumor stage and tumor biomarker expression. DNA hypermethylation and reduced expression of VWC2 were also detected in CRC cell lines HCT-116 and HT29. VWC2 overexpression suppressed the malignant growth of cells in vitro and in vivo. Co-immunoprecipitation and western blot assays showed that small ubiquitin-like modifier 1 (SUMO1) mediated SUMOylation of DNA methyltransferase 1 (DNMT1) and strengthened its protein stability, which promoted DNA methylation and suppression of the VWC2 gene. In summary, this study demonstrates that SUMO1-mediated activation of DNMT1 induces DNA methylation and downregulation of VWC2 in CRC to augment cancer development.

The association of decreased fecundity with insecticide resistance and the negative sublethal effects of insecticides on insect reproduction indicates the typical trade-off between two highly energy-demanding processes, detoxification and reproduction. However, the underlying mechanisms are poorly understood. The energy sensor adenosine monophosphate-activated protein kinase (AMPK) and the transcription factor Cap “n” collar isoform C (CncC) are important regulators of energy metabolism and xenobiotic response, respectively. In this study, using the beetle Tribolium castaneum as a model organism, we found that deltamethrin-induced oxidative stress activated AMPK, which promoted the nuclear translocation of CncC through its phosphorylation. The CncC not only acts as a transcription activator of cytochrome P450 genes but also regulates the expression of genes coding for ecdysteroid biosynthesis and juvenile hormone (JH) degradation enzymes, resulting in increased ecdysteroid levels as well as decreased JH titer and vitellogenin (Vg) gene expression. These data show that in response to xenobiotic stress, the pleiotropic AMPK–CncC signaling pathway mediates the trade-off between detoxification and reproduction by up-regulating detoxification genes and disturbing hormonal homeostasis.

To explore the mechanism of coadaptation and the potential drivers of pancreatic ductal adenocarcinoma (PDAC) metastasis to the liver, we study key molecules involved in this process and their translational value. Premetastatic niche (PMN) and macrometastatic niche (MMN) formation in a mouse model is observed via CT combined with 3D organ reconstruction bioluminescence imaging, and then we screen slit guidance ligand 2 (SLIT2) and its receptor roundabout guidance receptor 1 (ROBO1) as important factors. After we confirm the expression and distribution of SLIT2 and ROBO1 in samples from PDAC patients and several mouse models, we discover that SLIT2-ROBO1-mediated coadaptation facilitated the implantation and outgrowth of PDAC disseminated tumour cells (DTCs) in the liver. We also demonstrate the dependence receptor (DR) characteristics of ROBO1 in a follow-up mechanistic study. A neutralizing antibody targeting ROBO1 significantly attenuate liver metastasis of PDAC by preventing the coadaptation effect. Thus, we demonstrate that coadaptation is supported by the DR characteristics in the PMN and MMN.

The overactivation of osteoclasts in the endplate is one of the most important causes of low back pain (LBP) originating from endplate. Transforming growth factor-β family has been demonstrated to play an important role during osteoclast differentiation. GDF15 was reported to participate in several pathological states. In this study, we reported that the lumbar spine instability (LSI) induced the overactivation of osteoclasts and CD31hiEmcnhiendothelial vessels in the bony endplate. In addition, the expression of GDF15 in human disc samples and mice models were also increased. GDF15 could promote the fusion of preosteoclasts via Rac1/Cdc42/PAK/Cofilin axis, and facilitate the angiogenesis via the secretion of PDGF-BB. Furthermore, we proved that the GDF15 inhibitor, CTL-002 could reduce the expression of GDF15 in the endplate and alleviate the overactivation of osteoclasts and CD31hiEmcnhiendothelial vessels induced by LSI in vivo. In conclusion, we demonstrated that GDF15 could regulates the fusion of preosteoclasts and targeting GDF15 in the endplate served as a novel anabolic therapy for low back pain treatment.

Objective Previous studies have indicated that neurotransmitters play important roles in the occurrence and development of gastric cancer. MAOA is an important catecholamine neurotransmitter-degrading enzyme involvedin the degradation of norepinephrine, epinephrine and serotonin. To find a potential therapeutic target for the treatment of gastric cancer, the biological functions of MAOA and the underlying mechanism in gastric cancer need to be explored. Methods The Cancer Genome Atlas(TCGA), Gene Expression Omnibus (GEO) datasets, Kaplan‒Meier (KM) plotter and Oncomine databases were used to identify the differentially expressed genes, which mainly involved the degradation and synthesis enzymes of neurotransmitters in gastric cancer. We also investigated the expression pattern of MAOA in human and mouse tissues and cell lines by immunohistochemistry and Western blottinganalysis. Western blotting, quantitative real-time PCR, enzyme-linked immunosorbent assay (ELISA) and a Seahorse experiment were used to identify the molecular mechanism ofcancer cell glycolysis. MAOA expression and patientsurvival were analysed in the Ren Ji cohort, and univariate and multivariate analyses were performed based on the clinicopathological characteristics of the above samples. Results MAOA expression was significantly downregulatedin gastric cancer tissue and associated with poor patient prognosis. Moreover, the expression level of MAOA in gastric cancer tissue had a close negative correlation with theSUXmax valueof PET-CT in patients. MAOA suppressed tumour growth and glycolysis and promoted cancer cell apoptosis. We also show that MAOA can interact with NDRG1 and regulate glycolysis through suppression of the PI3K/Akt/mTOR pathway. MAOA expression may serve as an independent prognostic factor in gastric cancer patients. Conclusions MAOA attenuated glycolysis and inhibitedthe progression of gastric cancer through the PI3K/Akt/mTOR pathway. Loss of function or downregulation of MAOA can facilitate gastric cancer progression. Overexpression of MAOA and inhibition of the PI3K/Akt/mTOR pathway may provide a potential method for gastric cancer treatment in clinicaltherapeutic regimens.

Existing machine learning-based malware traffic recognition techniques can effectively detect abnormal behaviors in the network. However, almost all of them focus on a closed-set scenario in which the data used for training and testing come from the same label space. Since sophisticated malware and advanced persistent threats are evolving, it is impossible to exhaust all attacks to train a complete recognition model under the existing technical conditions. Therefore, recognition in the real network is an open-set problem, i.e., the recognition system should identify unknown and unseen attacks at test time. In this paper, we propose an uncertainty-aware method to identify known malicious traffic accurately and handle unknown traffic effectively. This method employs predictive uncertainty in deep learning as an indicator for unknown class detection. The predictive uncertainty represents the confidence in neural network predictions. In particular, the Deep Evidence Malware Traffic Recognition (DEMTR) model is presented to provide the multi-classification probability and predictive uncertainty in open-set scenarios using evidential deep learning. We demonstrate the performance of DEMTR on the MCFP dataset. Experimental results indicate that the proposed model outperforms the baseline methods in accuracy and F1-score.

Objective: Retention of serving members in the military may be increased through targeted psycho-social support of their families and dependents. This Defence funded study aimed to provide updated evidence on associations between current military service and the well-being of the member’s couple and relationships, to inform policy and practice. We conducted a rapid review of family and couple relationship qualities, comparing current serving samples with civilian, never-serving families. Method: We followed the Cochrane Rapid Review Method, searching publications from 2000. Outcomes were limited to modifiable factors of importance for policy related decision-making. Results: Four search strategies were constructed in Medline, PsycINFO, CINAHL and Cochrane CENTRAL. The review, in two parts, identified over 15,000 articles, of which only seven met the review criteria. The dearth of research identified reflected predominant focus on veteran rather than currently serving samples, and absence of comparison to a civilian group. We therefore also examined individual studies that closely approximated the inclusion criteria. Conclusions: The collated evidence offered four main findings: 1) A significant decrease in marital satisfaction for men and women with progressing stages of deployment; 2) Consistently higher prevalence of intimate partner violence for military versus civilian samples, growing with length of deployment, and mediated by histories childhood abuse or neglect; 3) Increased risk of psychological distress and problematic alcohol use by spouses of serving members, and 4) Barriers to engagement in therapeutic programs for military couples. Practice implications for screening and policy implications for targeted prevention efforts are discussed.

The taxonomic status of the Pieris napi-complex and similar species which occur in China are revised. Relevant species distributed in the adjacent regions were included to clarify the status of Chinese species and were briefly revised. All those species are described and illustrated and new synonyms are established. A molecular phylogenetic analysis is also performed on the species group including similar species, to investigate the phylogenetic relationships between taxa. Species of the Pieris napi-complex that occur in China and adjacent regions are redefined, with four similar species excluded (P. melaina, P. extensa, P. chumbiensis gyantsensis and P. melete). A distribution map and keys of the complex including similar species are provided. The taxon P. mihon Yakovlev, 2006 stat. nov. is raised from subspecies to species status; P. narina Verity, 1908 stat. rev. is confirmed as a distinct species rather than a subspecies of P. ochsenheimeri; Pieris euorientis Verity, 1908 stat. rev. is recovered as a distinct species sister to P. dulcinea. Two taxa, ssp. sauron and ssp. bryonides are moved from subspecies of P. euorientis and P. bryoniae, respectively, to P. napi, i.e. P. napi sauron Yakovlev, 2004 comb. nov and P. napi bryonides Sheljuzhko, 1910 comb. rev. A new synonym is proposed: Pieris ochsenheimeri tianshansis Tadokoro, Shinkawa & Wang, 2014, new synonym of P. mihon Yakovlev, 2006. A new mistaken identification is proposed: Pieris dulcinea kneitzi is a misidentification of Pieris erutae kneitzi Eitschberger, 1983 comb. rev. Five Chinese species belonging to the Pieris napi-complex were confirmed, namely P. narina, P. mihon, P. latouchei, P. dulcinea, and P. erutae. Among them, two species, P. mihon Yakovlev, 2006 and Pieris narina Verity, 1908, are newly recorded from China. The taxonomic status of Pieris steinigeri Eitschberger, 1983 and Pieris bryoniae sifanica Grum-Grshimailo, 1895 is also discussed.

Although many military families demonstrate resilience and strength, research highlights that military service may impact the health and wellbeing of families. In comparison with civilian families, military families are embedded within a broader military context and culture which may influence many aspects of family life, including socioeconomic status and social participation. This rapid review utilised a systematic methodology to synthesise the evidence of comparing possible differences of the socioeconomic and social participation of military families with civilian families. Relevant online databases such as Medline, PsycINFO, CINAHL and ProQuest Central were searched for articles published between January 2000 and February 2022. After screening 3057 articles, five studies were included for analysis. The results highlight considerable income, education and employment gaps between current serving military and civilian spouses. An association was found between social, economic status and increased risk of violence or assaults in military families. Specifically, younger age and decline in health status were key predictors of domestic violence assaults in military families. This review highlights emerging evidence and recommends further Australian-based research with military families. Policy, research, and practice implications are discussed with consideration to preventative interventions tailored towards strengthening health, wellbeing, and socio-economic status of military families.

Background Mental health problems are important public health issues among college students and are associated with various social factors. However, these influencing factors were scarcely summarized in Chinese college students comprehensively. This study aims to assess the associations between socio-demographic characteristics, lifestyles, social support quality (SSQ) and mental health among Chinese college students . Methods A cross-sectional study was conducted in Wuhan, China, from October 2017 to February 2018. College students from 18 colleges or universities were randomly recruited using multi-stage cluster sampling method. The Multidimensional Scale of Perceived Social Support scale and 12-items General Health Questionnaire were used to estimate students’ SSQ and mental health statuses, respectively. Logistic regression analysis was used to evaluate the associations between socio-demographic characteristics, lifestyles, SSQ and mental health problems. Results A total of 10,676 college students were included. Among them, 21.4% were identified as having possible mental health problems. Students being a female, aged 18–22 years old, whose mother held college degrees and above, and drinking alcohol were more likely to have mental health problems (P P Conclusion Besides socio-demographic and lifestyle factors, social support is a critical factor for mental health among college students. Improving SSQ, especially which from the family, could be an effective method to prevent mental health problems among college students.