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Background: Adhesion G protein-coupled receptors (aGPCRs), a distinctive subset of the G protein-coupled receptor (GPCR) superfamily, play crucial roles in various physiological and pathological processes, with implications in tumor development. Despite the global prevalence of breast cancer (BRCA), specific aGPCRs as potential drug targets or biomarkers remain underexplored. Methods: UALCAN, GEPIA, Kaplan–Meier Plotter, MethSurv, cBiopportal, String, GeneMANIA, DAVID, Timer, Metascape, and qPCR were applied in this work. Results: Our analysis revealed significantly increased transcriptional levels of ADGRB2, ADGRC1, ADGRC2, ADGRC3, ADGRE1, ADGRF2, ADGRF4, and ADGRL1 in BRCA primary tumors. Further analysis indicated a significant correlation between the expressions of certain aGPCRs and the pathological stage of BRCA. High expression of ADGRA1, ADGRF2, ADGRF4, ADGRG1, ADGRG2, ADGRG4, ADGRG6, and ADGRG7 was significantly correlated with poor overall survival (OS) in BRCA patients. Additionally, high expression of ADGRF2 and ADGRF4 indicated inferior recurrence-free survival (RFS) in BRCA patients. The RT-qPCR experiments also confirmed that the mRNA levels of ADGRF2 and ADGRF4 were higher in BRCA cells and tissues. Functional analysis highlighted the diverse roles of aGPCRs, encompassing GPCR signaling and metabolic energy reserves. Moreover, aGPCRs may exert influence or actively participate in the development of BRCA through their impact on immune status. Conclusion: aGPCRs, particularly ADGRF2 and ADGRF4, hold promise as immunotherapeutic targets and prognostic biomarkers in BRCA. [ABSTRACT FROM AUTHOR]

Predicting the likelihood vascular events in patients with BCR/ABL1-negative myeloproliferative neoplasms (MPN) is essential for the treatment of the disease. However, effective assessment methods are lacking. Thrombin-antithrombin complex (TAT), plasmin-α2- plasmininhibitor complex (PIC), thrombomodulin (TM), and tissue plasminogen activator-inhibitor complex (t-PAIC) are the new direct indicators for coagulation and fibrinolysis. The aim of this study was to investigate the changes of these four new indicators in thrombotic and hemorrhagic events in BCR/ABL1-negative MPN. The study cohort of 74 patients with BCR/ABL negative myeloproliferative disorders included essential thrombocythemia, polycythemia vera, and primary myelofibrosis (PMF). A panel of 4 biomarkers, including TAT, PIC, TM, and t-PAIC were determined using Sysmex HISCL5000 automated analyzers, whereas fibrin/fibrinogen degradation products (FDP), D-dimer and Antithrombin III (ATIII) were analyzed using Sysmex CS5100 coagulation analyzer. A total of 24 (32.4%) patients experienced thrombotic events and hemorrhagic events occurred in 8 patients (10.8%). Compared to patients without hemorrhagic-thrombotic events, patients with thrombotic events had higher fibrinogen (FIB) level, FDP level and lower ATIII activity, while patients with hemorrhagic events had lower white blood cell count and hemoglobin level, higher FDP level (P < 0.05). Patients with a JAK2V617F mutation were more likely to experience thrombotic events (P < 0.05). In addtion, patients with thrombotic events had higher TAT, PIC, TM, and t-PAIC levels than patients without hemorrhagic-thrombotic events (P < 0.05), whereas patients with hemorrhagic events had a lower median value in TAT and TM (no statistical difference, P > 0.05). Patients with higher TAT, TM and t-PAIC were more likely to experience thrombotic events (P < 0.05), and only TAT was positively correlated with thrombotic events (Spearman r =0.287, P = 0.019). TAT, PIC, TM, and t-PAIC combined with ATIII and FDP have a certain value for predicting thrombosis in patients with BCR/ABL1-negative MPN. These 6 parameters are worth further exploration as predictive factors and prognostic markers for early thrombotic events. [ABSTRACT FROM AUTHOR]

Purpose: Chimeric antigen receptor (CAR) T cell therapy has achieved great success in treating hematologic malignancies. However, it is yet to prove effective in the treatment of solid tumors. Thus, it is necessary to develop appropriate methodology for the long-term, accurate, and quantitative evaluation of the distribution and activities of CAR T cells in solid tumors. In the present study, we engineered TfR ΔPSMA CAR (CAR-ΔPSMA) T cells, which targeted the transferrin receptor (TfR) expressed by tumor cells and could be tracked in vivo via a reporter gene encoding the truncated prostate specific membrane antigen (ΔPSMA). We then quantitatively monitored these CAR T cells in vitro and in vivo using [68Ga]Ga-PSMA-617 positron emission tomography (PET)/computed tomography (CT). Methods: The CAR-ΔPSMA T cells were genetically engineered by transducing T cells with a lentiviral vector encoding TfR41BBζ-T2A-ΔPSMA. Firstly, the target expression, activation, and cytotoxicity of CAR-ΔPSMA T cells were validated in vitro. Secondly, the minimum thresholds of CAR-ΔPSMA T cells detection for [68Ga]Ga-PSMA-617 PET/CT were also determined in vitro and in vivo respectively. Lastly, the feasibility of monitoring the biodistribution and infiltration of CAR-ΔPSMA T cells after systematic administration was evaluated in the breast cancer subcutaneous xenograft model. Results: The CAR-ΔPSMA T cells retained activation and tumor killing capacity after transduction of the ΔPSMA-encoding reporter gene. Next, the CAR-ΔPSMA T cells could be reliably tracked by [68Ga]Ga-PSMA-617 PET/CT, the detection sensitivity of which was 250 cells/mm3 in vitro and 100 cells/mm3 in vivo. Next, the sequential imaging assays revealed that [68Ga]Ga-PSMA-617 PET/CT could be used to specifically visualize ΔPSMA+ CAR T cells at the tumor site. The increase in the [68Ga]Ga-PSMA-617 signal intensity over time allowed us to effectively detect CAR T cells in vivo. Conclusion: Our findings preliminarily confirmed that [68Ga]Ga-PSMA-617 PET/CT could reliably detect CAR-ΔPSMA T cells in vitro and in vivo in solid tumors, laying the foundation for the monitoring CAR T cell therapy in the future. [ABSTRACT FROM AUTHOR]

Peroxicedoxin 4 (PRDX4), a member of the peroxicedoxins (PRDXs), has been reported in many cancer-related studies, but its role in uterine corpus endometrial carcinoma (UCEC) is not fully understood. In the present study, we found that PRDX4 was highly expressed in UCEC tissues and cell lines through the combination of bioinformatics analysis and experiments, and elevated PRDX4 levels were associated with poor prognosis. Knockdown of PRDX4 significantly blocked the proliferation and migration of the UCEC cell line Ishikawa and reduced degree of cell confluence. These findings highlight the oncogenic role of PRDX4 in UCEC. In addition, genes that interact with PRDX4 in UCEC were MT-ATP8, PBK, and PDIA6, and we speculated that these genes interacted with each other to promote disease progression in UCEC. Thus, PRDX4 is a potential diagnostic biomarker for UCEC, and targeting PRDX4 may be a potential therapeutic strategy for patients with UCEC. [ABSTRACT FROM AUTHOR]

In order to study the theoretical mechanism of the impact of green technology progress on carbon emissions, this article constructs a theoretical mechanism of the impact of green technology progress on carbon emission growth. Explore the conditions for achieving carbon peak and carbon reduction. Based on the Cobb Douglas production function, construct a three sector model that includes capital, labor, and energy. Empirical methods were used to analyze the quantitative impact of green technology progress on carbon emission growth and the moderating effect of energy input share. This study mainly used provincial panel data from 1995 to 2020. Calculate carbon dioxide emissions based on energy consumption and carbon dioxide emission coefficients of various energy sources in different regions. Using the perpetual inventory method to calculate capital growth rate, green computing progress rate, etc., to provide data support for the green technology carbon reduction model. Empirical analysis of the impact of green technology progress on carbon emissions using the FGLS panel model. Theoretical and empirical analyses show that green technological progress promotes an increase in the carbon emission growth rate through the scale effect, with an impact coefficient of 0.607; it promotes a decrease in the carbon emission growth rate through the technological effect, with an impact coefficient of − 0.667; the combined effect promotes a decrease in growth rate of carbon emissions, with an impact coefficient of − 0.06. The share of energy inputs has a positive regulating effect on the scale effect. [ABSTRACT FROM AUTHOR]

Purpose: The aged microenvironment plays a crucial role in tumor onset and progression. However, it remains unclear whether and how the aging of the extracellular matrix (ECM) influences cancer onset and progression. Furthermore, the mechanisms and implications of extracellular matrix senescence-related genes (ECM-SRGs) in pan-cancer have not been investigated. Methods: We collected profiling data from over 10,000 individuals, covering 33 cancer types, 750 small molecule drugs, and 24 immune cell types, for a thorough and systematic analysis of ECM-SRGs in cancer. Results: We observed a significant correlation between immune cell infiltrates and Gene Set Variation Analysis enrichment scores of ECM-SRGs in 33 cancer types. Moreover, our results revealed significant differences in immune cell infiltration among patients with copy number variations (CNV) and single nucleotide variations (SNV) in ECM-SRGs across various malignancies. Aberrant hypomethylation led to increased ECM-SRGs expression, and in specific malignancies, a connection between ECM-SRGs hypomethylation and adverse patient survival was established. The frequency of CNV and SNV in ECM-SRGs was elevated. We observed a positive correlation between CNV, SNV, and ECM-SRGs expression. Furthermore, a correlation was found between the high frequency of CNV and SNV in ECM-SRGs and poor patient survival in several cancer types. Additionally, the results demonstrated that ECM-SRGs expression could serve as a predictor of patient survival in diverse cancers. Pathway analysis unveiled the role of ECM-SRGs in activating EMT, apoptosis, and the RAS/MAPK signaling pathway while suppressing the cell cycle, hormone AR, and the response to DNA damage signaling pathway. Finally, we conducted searches in the "Genomics of Drug Sensitivity in Cancer" and "Genomics of Therapeutics Response Portal" databases, identifying several drugs that target ECM-SRGs. Conclusions: We conducted a comprehensive evaluation of the genomes and immunogenomics of ECM-SRGs, along with their clinical features in 33 solid tumors. This may provide insights into the relationship between ECM-SRGs and tumorigenesis. Consequently, targeting these ECM-SRGs holds promise as a clinical approach for cancer treatment. [ABSTRACT FROM AUTHOR]

Although a wide variety of background subtraction methods has been proposed in recent years, none has been able to fully address multi-scale moving objects and dynamic background in real surveillance tasks. In this paper, a novel and effective background subtraction method, named regional multi-feature-frequency (RMFF), is proposed to detect multi-scale moving objects under dynamic background. Unlike many existing methods construct background model using simple multi-feature combinations, RMFF exploits the spatiotemporal cues of multi-feature as well as superpixels at each scale, thus allowing for more robust information to be exploited for background modeling. Specifically, the spatial relationship between pixels in a neighborhood and the frequencies of features over time are first exploited, enabling accurate detection of moving objects while ignoring most dynamic background changes. Then, the use of multi-scale superpixels for exploiting the structural information existing in real-world scenes further enhances robustness to multi-scale objects and environmental variations. Finally, an adaptive strategy is employed to dynamically adjust the foreground/background segmentation threshold for each region without user intervention. This adaptive threshold is defined for each region separately, and can adjust dynamically based on continuous monitoring of the background changes, thereby effectively reducing potential segmentation noise. Experiments on the 2014 version of the ChangeDetection.net dataset demonstrate that the proposed method outperforms the 12 state-of-the-art algorithms in terms of overall F-Measure and performs effectively in many complex scenes. Consequently, it is verified that the developed approach is feasible and useful for robust application in practical video surveillance. [ABSTRACT FROM AUTHOR]

Objective: The relationship between vascular compression of the vestibulocochlear nerve and audio-vestibular symptoms remains controversial. We aimed to examine the radiological features of vascular loops signs in cerebellopontine angle (CPA) and internal auditory canal (IAC) in patients with unilateral Ménière's disease (MD). Methods: One hundred and thirty-seven patients with unilateral definite MD and 69 control subjects (138 ears) were enrolled. All subjects received magnetic resonance imaging of CPA-IAC. The configuration of vascular loops in CPA-IAC, based on the Kazawa classification system, from MD-affected, non-affected and control ears were compared. The associations between imaging findings and Ménière's stage, electrocochleogram (EcochG) and caloric test were analyzed. Results: (1) Among the MD-affected ears, 6 cases (4.4%) were classified as Kazawa type IA, 27 cases (19.7%) as IB, 60 cases (43.8%) as IIA, and 44 cases (32.1%) as IIB. No significant interaural difference in the distribution of Kazawa's types was found ( x 2 = 4.737, p = 0.578) in unilateral MD patients. (2) The distribution of Kazawa's types were not significantly different between the MD-affected ears and the control subjects ( x 2 = 2.876, p = 0.411). (3) No relationship was found between Kazawa staging of the MD-affected ear and Ménière's stage (H = 2.679, p = 0.444), EcochG ( x 2 = 0.827, p = 0.867) and caloric test ( x 2 = 4.116, p = 0.248). Conclusions: In patients with unilateral MD, the configuration of vascular loops in CPA-IAC region, measured by Kazawa criteria, did not correlate with the laterality, clinical stage, the results of EcochG and caloric test, suggesting that vascular loops may be natural anatomical variations for patients with MD. [ABSTRACT FROM AUTHOR]

Background: Bone marrow mesenchymal stem cells (BMSCs) can differentiate into osteoblasts and thus present a tremendous therapeutic potential in osteoporosis. Here, we elucidated the involvement of long non-coding RNAs (lncRNAs) HOXA transcript antisense RNA, myeloid-specific 1 (HOTAIRM1) in the osteogenic differentiation of BMSCs. Methods and results: The expression levels of HOTAIRM1, miR-152-3p, ETS proto-oncogene 1 (ETS1), runt-related transcription factor 2 (RUNX2), Osterix, and osteocalcin (OCN) were determined by a quantitative real-time polymerase chain reaction (qRT-PCR) or western blot method. Targeted relationship between miR-152-3p and HOTAIRM1 or ETS1 was confirmed by dual-luciferase reporter and RNA pull-down assays. The activity of alkaline phosphatase (ALP) was measured by the ALP Activity Assay Kit. The extent of the calcium deposition was assessed by Alizarin Red Staining. Our data showed that HOTAIRM1 and ETS1 levels were up-regulated and miR-152-3p expression was down-regulated during osteogenic differentiation of human BMSCs (HBMSCs). HOTAIRM1 overexpression enhanced osteogenic differentiation of HBMSCs, and decreased level of HOTAIRM1 suppressed osteogenic differentiation of HBMSCs. HOTAIRM1 directly targeted miR-152-3p. ETS1 was identified as a direct and functional target of miR-152-3p. Furthermore, HOTAIRM1 functioned as a post-transcriptional regulator of ETS1 expression by miR-152-3p. Conclusion: The findings in this paper identify HOTAIRM1 as a novel regulator of osteogenic differentiation of BMSCs by the regulation of miR-152-3p/ETS1 axis, uncovering HOTAIRM1 as a promising therapeutic strategy for osteoporosis. [ABSTRACT FROM AUTHOR]

Purpose: γδ T cell–based immunotherapy has been rolled out as a promising treatment strategy for malignant tumors due to their potent anti-tumor cytotoxicity, ease of expansion, and unrestricted MHC feature. However, the dynamics and outcomes of γδ T cells in tumor sites are poorly understood. Reported strategies rely on ex vivo biolabeling, significantly limiting the application of γδ T cell molecular imaging. Herein, we investigated whether VLA-4 (very late antigen-4), a crucial component in the effective trafficking of lymphocytes, could serve as a biomarker to non-invasively visualize γδ T cells. Methods: VLA-4-targeted tracer, 68 Ga-LLP2A, was evaluated in MDA-MB-231- and A549-bearing mice with adoptive transfer of γδ T cells by longitudinal PET/CT imaging. Imaging data were verified by ex vivo biodistribution studies, and the co-localization of CD3 and VLA-4 was validated by immunohistochemistry studies. Results: 68 Ga-LLP2A showed high specificity to VLA-4-expressing γδ T cells in both in vitro and tumor-bearing mice with adoptive transfer of γδ T cells. Longitudinal PET imaging of 68 Ga-LLP2A in tumor-bearing mice with adoptive transfer of γδ T cells showed an increasing tumor tracer uptake, revealing the tumor-specific homing of γδ T cells. The presence of VLA-4-expressing γδ T cells in tumors was confirmed via histological analysis. Conclusion: To the best of our knowledge, we reported the first molecular probe, 68 Ga-LLP2A, for in vivo imaging of γδ T cells in live tumors, which advances PET imaging of γδ T cells and supports the translation of imaging agents for immunotherapeutic monitoring. [ABSTRACT FROM AUTHOR]

Objective: Radiological anatomical variations, measured by magnetic resonance imaging (MRI), were evaluated in patients with ipsilateral delayed endolymphatic hydrops (DEH) and unilateral Ménière's disease (MD). The role of anatomical variations in different subtypes of hydropic ear disease was investigated. Methods: Twenty-eight patients with ipsilateral DEH, 76 patients with unilateral MD, and 59 control subjects were enrolled. The radiological indices included the distance between the vertical part of the posterior semicircular canal and the posterior fossa (MRI-PP distance) and the visibility of vestibular aqueduct (MRI-VA). These variations among patients with DEH, MD, and control subjects were compared. The correlation between radiological anatomical variations and clinical features or audio-vestibular findings was also examined. Results: (1) MRI-PP distance in the affected side of unilateral MD was shorter than that in ipsilateral DEH (Z = − 2.481, p = 0.013) and control subjects (Z = − 2.983, p = 0.003), while the difference of MRI-PP distance between the affected side of ipsilateral DEH and control subjects was not statistically significant (Z = − 0.859, p = 0.391). (2) There was no significant interaural difference of MRI-PP distance in patients with unilateral MD (Z = − 0.041, p = 0.968) and ipsilateral DEH (t = − 0.107, p = 0.915) respectively. (3) No significant interaural difference of MRI-VA visibility was observed in patients with unilateral MD (χ2 = 0.742, p = 0.389) and ipsilateral DEH (χ2 = 0.327, p = 0.567) respectively. (4) No correlation was found between these anatomical variables and clinical features or audio-vestibular findings in patients with unilateral MD and ipsilateral DEH respectively (p > 0.05). Conclusions: Anatomical variations of inner ear may be a predisposing factor in the pathogenesis of unilateral MD rather than ipsilateral DEH. Key Points: • Patients with ipsilateral delayed endolymphatic hydrops showed normal distance between the vertical part of the posterior semicircular canal and the posterior fossa. • Compared to patients with ipsilateral delayed endolymphatic hydrops and control subjects, patients with unilateral Ménière's disease exhibited shorter distance between the vertical part of the posterior semicircular canal and the posterior fossa. • Anatomical variations of inner ear may be a predisposing factor in the pathogenesis of unilateral Ménière's disease rather than ipsilateral delayed endolymphatic hydrops. [ABSTRACT FROM AUTHOR]

The excavation face stability is a critical issue in the analysis of the tunneling disturbance to the surrounding environment, in which the soil arching effect is a phenomenon that cannot be ignored. Based on the wedge-prism model, this study proposed a slice method to calculate the limit support pressure, taking into account both the vertical soil arching effect of the prism and the horizontal arching effect of the wedge. In addition, the rotation of the principal stress was introduced to improve the lateral stress ratio on the vertical sliding faces including the wedge and the prism, in which two new trajectories of the major principal stress were recommended, based on a previous numerical study. Furthermore, the contribution of the incomplete soil arching effect was discussed in this study, assuming that there was a function between the effective internal friction angle of the soil and the tunnel cover depth. Through the comparison of the results with theoretical and numerical models, the improved model was validated and showed agreement with them. Finally, parameters related to the limit support pressure were thoroughly investigated to provide a better understanding of the proposed model. [ABSTRACT FROM AUTHOR]

Objective: To evaluate the predictive value of gadoxetic acid-enhanced MRI features (focused on Liver Imaging Reporting and Data System (LI-RADS) v2018 features and non-LI-RADS imaging features) for microvascular invasion (MVI) of hepatocellular carcinoma (HCC). Methods: From October 2018 to December 2020, 134 patients who underwent gadoxetic acid-enhanced MRI with a pathological diagnosis of HCC after hepatectomy were enrolled in this retrospective study. Two radiologists assessed the pre-hepatectomy LI-RADS v2018 imaging features and non-LI-RADS features to identify independent predictors of MVI of HCC with a logistic regression model. Results: Four MRI features were found to be independent predictors of MVI: corona enhancement [odds ratio (OR) 5.787; 95% confidence interval (CI) 1.180, 28.369; p = 0.030], mosaic architecture (OR 7.097; 95% CI 1.299, 38.783; p = 0.024), nonsmooth tumor margin (OR 13.131; 95% CI 3.950, 43.649; p < 0.001), and peritumoral hypointensity on hepatobiliary phase (HBP) (OR 33.123; 95% CI 2.897, 378.688; p = 0.005). When one of four imaging features was present, the sensitivity was 93.2% (41/44), and the specificity was 71.1% (64/90). Conclusion: The four imaging features including corona enhancement, mosaic architecture, nonsmooth tumor margin, and peritumoral hypointensity on HBP can be used as preoperative imaging biomarkers for predicting MVI in patients at high risk for HCC. When one of the four imaging features is present, MVI can be predicted with a sensitivity > 90%. [ABSTRACT FROM AUTHOR]

Pyroptosis is a programmed cell death process which is accompanied by inflammation. The aims of this in vitro and in vivo study were to reveal whether miR-129 contributed to neuronal pyroptosis and cognitive impairment and to further explore its mechanism involved. PC-12 cells were treated with LPS, miR-129 antagomir, AXL1717 (IGF-1 receptor blocker), or SB216763 (GSK3β blocker). After that, expression of miR-129 was measured using qRT-PCR. Relationship between miR-129 and IGF-1 was revealed using luciferase reporter assay. Protein expression of IGF-1, p-Ser9-GSK3β, NLRP3, and Caspase-1 was determined using western blotting. Pyroptosis rate was measured using flow cytometry. Wistar rats were fed with high-fat diet to induce neural inflammation and were further treated with miR-129 antagomir through intracerebroventricular injection. Then, cognitive impairment was assessed by water maze test. Expression of the proteins mentioned above was measured again in midbrain and hippocampus of the rats. In the PC-12 cells, LPS-induced neuronal pyroptosis can be alleviated by miR-129 antagomir. IGF-1 was a specific target for miR-129. Up-regulation and down-regulation of IGF-1/GSK3β signaling pathway separately alleviated and deteriorated neuronal pyroptosis in the cells. In the rats, high-fat diet caused cognitive impairment following with neuronal pyroptosis and down-regulation of IGF-1/GSK3β signaling pathway in midbrain and hippocampus tissues. Also, miR-129 antagomir improved these abnormalities in the rats. Inhibition of miR-129 improved neuronal pyroptosis and cognitive impairment through IGF-1/GSK3β signaling pathway. [ABSTRACT FROM AUTHOR]

This study extends the social influence factor in the Unified Theory of Acceptance and Use of Technology (UTAUT) model by delineating it into coercive, normative, and mimetic pressures based on institutional theory. It investigates the role of each institutional pressure in influencing the behavioural intention of accounting lecturers in Malaysia's public universities to use Information and Communications Technology (ICT)-enhanced student-centred teaching methods. Using a purposive sampling method, self-report questionnaires were distributed to accounting lecturers in Malaysia's public universities offering undergraduate accounting programmes. This resulted in 114 usable questionnaires. The hypothesized relationships were tested using structural equation modeling via Smart-PLS software. Only coercive and normative pressures were found to have a significant and positive influence on behavioural intention. Mimetic pressures had an insignificant influence on behavioural intention. The findings of this study are useful to authorities in the higher education sector and practitioners who have been encouraging the student-centred teaching movement. This study provides further enlightenment on which social factors yield the most effects at the present moment and which social factors need greater work to yield better effects on increasing lecturers' behavioural intentions as a whole. [ABSTRACT FROM AUTHOR]

Inflammation contributes to mitochondrial dysfunction and neuronal apoptosis. The aim of this study was to determine whether insulin-like growth factor-1 (IGF-1) alleviates mitochondrial apoptosis in lipopolysaccharide (LPS)-treated PC-12 cells, and to further explore the mechanism involved. Prepared PC-12 cells were treated with IGF-1, Mdivi-1 (DRP1 blocker), LY294002 (PI3K blocker), betulinic acid (NF-κB activator) or their combinations. Mitochondrial membrane potential and ATP generation were then measured to assess mitochondrial function. The rate of apoptosis was determined using flow cytometry. The expression of several apoptosis proteins (i.e. Bax, cleaved caspase-9 and cleaved caspase-3) and signaling proteins (i.e. p-GSK3β, NF-κB and NLRP3) was measured using western blotting. Compared with the control cells, the LPS-treated cells showed evidence of mitochondrial dysfunction, increased apoptosis and upregulation of apoptosis proteins, which were significantly alleviated by Mdivi-1. These findings indicate that neuronal apoptosis was activated partly through the mitochondrial pathway. IGF-1 treatment inhibited mitochondrial apoptosis in a dose-dependent manner in the LPS-treated cells. The reagent also increased the expression of p-GSK3β and decreased the expression of NF-κB and NLRP3. Both LY294002 and betulinic acid reversed the protective effect of IGF-1. In addition, LY294002 affected the expression of the three signaling proteins, while betulinic acid only affected the expression of NF-κB and NLRP3. These findings indicated a GSK3β/NF-κB/NLRP3 signaling pathway was existed and was involved in the protective mechanism of IGF-1. In conclusion, IGF-1 alleviated mitochondrial apoptosis through GSK3β/NF-κB/NLRP3 signaling pathway in LPS-treated PC-12 cells. [ABSTRACT FROM AUTHOR]

Hydrothermal carbonization (HTC) combined with pelletization is an efficient upgrading process to convert biomass into energy-dense pellets. Binders usually serve an important role in the quality of biofuel pellets. Here, hydrochar was produced from tobacco stem through HTC, and was pelletized in the presence of various binders. The effect of four kinds of binders (K2CO3, CaCO3, xanthan gum and carboxymethyl cellulose) on the basic fuel properties, mechanical strength, moisture adsorption and combustion characteristics was investigated. The results showed that K2CO3 assisted pellet had decreased compressive strength, increased hygroscopicity and high combustion residues. The compressive strength of pellets increased with increasing amount CaCO3 binder probably due to the hardening effect of enhanced adhesion attraction forces between adjacent particles. Meanwhile, the CaCO3 assisted pellet exhibited the lowest moisture uptake behavior. In addition, the introduction of organic binders led to improved mechanical strength, especially for xanthan binder, which could be ascribed to the formation of solid bridges and enhancement of adhesion forces between particles. TGA results suggested that the binder-assisted pellets exhibited desirable combustion characteristics such as decreased ignition temperature and increased comprehensive combustibility index. Kinetic parameters of the combustion process of binder-assisted pellets were also determined by employing the model free isoconversional Kissinger–Akahira–Sunose method. This study demonstrated that HTC of tobacco stem combined with pelletization in the presence of appropriate binders provide an alternative for solid biofuel pellets production. Hydrothermal carbonization (HTC) of tobacco stem combined with pelletization in the presence of appropriate binders provide an alternative for solid biofuel pellets production. [ABSTRACT FROM AUTHOR]

Background and aims: Liver injury is found in some of patients with COVID-19. Liver injury of COVID-19 patients based on severity grading and abdominal radiological signs have not been reported until now. The aim of our study is to determine clinical profiles of the patients based on severity grading, describe abdominal radiological signs, and investigate the correlations of the severity with clinical profiles and radiological signs. Methods: This retrospective cohort study included 115 patients with COVID-19 from Jan 2020 to Feb 2020. Medical records of the patients were collected and CT images were reviewed. Results: Common clinical manifestations of patients with COVID-19 were fever (68.70%), cough (56.52%), fatigue (31.30%); some of them had gastrointestinal symptoms (diarrhea, 12.17%; nausea or vomiting 7.83%; inappetence, 7.83%). Abnormal liver function was observed in some of patients with COVID-19. Significant differences in the levels of AST, albumin,CRP were observed among different groups classified by the severity. Common findings of upper abdominal CT scan were liver hypodensity (26.09%) and pericholecystic fat stranding (21.27%); liver hypodensity was more frequently found in critical cases (58.82%). The severity of COVID-19 correlated with semi-quantitative CT score of pulmonary lesions, CT-quantified liver/spleen attenuation ratio in patients with COVID-19. Conclusions: Some of the patients with COVID-19 displayed liver damage revealed by liver functional tests and upper abdominal CT imaging, and the severity of COVID-19 patients correlated with some of liver functional tests and CT signs; thus, it will allow an earlier identification of high-risk patients for early effective intervention. [ABSTRACT FROM AUTHOR]

Tobacco residues produced from domestic cigarette industry are an abundant biomass resource which have the potential to be exploited and utilized as solid fuel. In the present study, a comprehensive investigation was performed on the fuel properties of hydrochars which were derived from hydrothermal carbonization (HTC) of tobacco residues in the presence of minute amount of graphene oxide (GO). The effect of HTC temperature and residence time on the chemical compositions, structure, and combustion performance of the resultant GO-assisted hydrochars was evaluated. The carbon content and energy densification increased with the hydrothermal treatment intensity accompanying with the decline in hydrogen and oxygen contents. Meanwhile, the combustion behavior of hydrochars was analyzed based on the thermogravimetric curves and isoconversional Kissinger-Akahira-Sunose method. The activation energy varied with conversion degrees for the tested samples, indicating the complexity of hydrochar combustion. Notably, the decreased activation energies for GO-assisted hydrochars may indicate the catalytic role of GO during the combustion process of components in hydrochars. [ABSTRACT FROM AUTHOR]

In our recent study, we observed consistent increases in miR-124-3p levels in exosomes derived from cultured BV2 microglia which was treated with repetitive traumatic brain injury (rTBI) mouse model brain extracts. To clarify the mechanisms underlying increases in microglia-derived exosomal miR-124-3p and their role in regulating neuronal autophagy after TBI, we investigated the impact of exosomal miR-124-3p on neuronal autophagy in scratch-injured HT22 neurons and rTBI mice. We harvested injured brain extracts from rTBI mice at 3 to 21 days post injury (DPI) for the treatment of cultured BV2 microglia in vitro. We observed significant induction of autophagy following TBI in vitro, and that inhibition of activated neuronal autophagy could protect against trauma-induced injury. Our results indicated that co-culture of injured HT22 neurons with miR-124-3p overexpressing BV2 microglia exerted a protective effect by inhibiting neuronal autophagy in scratch-injured neurons. Further research revealed that these effects were achieved mainly via upregulation of exosomal miR-124-3p, and that Focal adhesion kinase family-interacting protein of 200 kDa (FIP200) plays a key role in trauma-induced autophagy. Injection of exosomes into the vena caudalis in in vivo experiments revealed that exosomal miR-124-3p was associated with decreases in the modified neurological severity score (mNSS) and improvements in Morris water maze (MWM) test results in rTBI mice. Altogether, our results indicate that increased miR-124-3p in microglial exosomes following TBI may inhibit neuronal autophagy and protect against nerve injury via their transfer into neurons. Thus, treatment with microglial exosomes enriched with miR-124-3p may represent a novel therapeutic strategy for the treatment of nerve injury after TBI. [ABSTRACT FROM AUTHOR]

A correction is presented to the article "European Journal of Nuclear Medicine and Molecular Imaging" which appeared in the 18 July 2022 issue.

This study assessed the effectiveness of limestone-montmorillonite-rapeseed residue-Si fertilizer compound amendment on the bioavailability and crop uptake of cadmium (Cd) and enzyme activities in acidic paddy soils. Applying the compound amendment at ratios of 1%-3% increased soil pH by 0.1-1.9 units, decreased leaching ratios of soil Cd 4.0%-22%, and decreased exchangeable and carbonated Cd 42%-55% and 27%-49%, respectively. Organic matter-bound Cd increased 47%-62% (p < 0.05). Cadmium concentrations decreased in the roots, culms, leaves, and grains of rice grown in the Cd-contaminated soils by 37%-81%, 18%-73%, 29%-64% and 27%-63%, respectively, (p < 0.05). Catalase and urease activities increased 2.5%-63% and 3.9%-36%, (p < 0.05), respectively. Applying this compound amendment may significantly mitigate soil acidification and decrease the bioavailability and crop uptake of Cd in acidic Cd-contaminated paddy soils. [ABSTRACT FROM AUTHOR]

The source and sink landscape patterns refer to landscape types or units that can either promote positive evolvement of non-point source (NPS) pollution process, or can prevent/defer the ecological process, respectively. Therefore, the role of a catchment landscape pattern in nutrient losses can be identified based on the spatial arrangement of source and sink landscapes. To reveal the relations between landscape spatial characteristics and NPS pollution in small catchment, a case study was carried out in a Wangjiagou small catchment of the Three Gorges Reservoir Region (TGRR), China. Google earth imagery for 2015 were processed and used to differentiate source and sink landscape types, and six subcatchments were selected as sample regions for monitoring nitrogen and phosphorus nutrients. Relative elevation, slope gradient and relative flow length was used to construct the Lorenz curves of different source and sink landscape types in the catchment, in order to assess the source and sink landscape spatial characteristics. By calculating the location-weighted landscape indices of each subcatchment and total catchment, the landscape spatial load characteristics affecting the NPS pollution was identified, with a further Pearson correlation analysis for location-weighted landscape indices and nitrogen-phosphorus monitoring indicators. The analysis of Lorenz curve has revealed that the obtained distribution trend of Lorenz curve and curve area quantified well the spatial characteristics of source and sink landscape pattern related to the relative elevation, slope gradient and relative flow length in small catchment. Results of Pearson correction analysis indicated that location-weighted landscape index (LWLI) combining of terrain and landscape type factor did better in reflecting the status of nitrogen and phosphorus loss than the indices related to relative elevation, slope gradient and relative flow length. [ABSTRACT FROM AUTHOR]

Although, there is growing awareness in the progressive neurodegeneration of chronic traumatic encephalopathy, changes of immune reactions remain equivocal at best. Thus, in a clinically relevant rat repetitive mild traumatic brain injury (rmTBI) model, some immunologic cells (T cell subsets, microglia) in the injured brain and peripheral blood were analyzed by flow cytometry and immunofluorescence. In the injured brain, CD3 T cells showed a bimodal increase during 42 days post-injury (dpi). CD3CD4 T cells firstly increased and then decreased, while CD3CD8 T cells had reversed tendency. CD86/CD11b M1-like microglia increased at 42 dpi and CD206/CD11b M2-like microglia peaked at 7 dpi. In addition, peripheral immune suppression was implicated in the chronic phase after rmTBI. Taken together, the study provided useful information on long-term dynamic changes of some immune cells after rmTBI in rats. [ABSTRACT FROM AUTHOR]

Objective: To assess the safety and immunogenicity of pneumococcal conjugate vaccine (PCVs) in preterm infants.Methods: In accordance with the PRISM (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) statement (as of May 2015), a meta-analysis was conducted to evaluate the safety and immunogenicity of PCVs in preterm infants.Results: Ten thousand nine hundred sixty full-term infants and 2131 preterm infants with 344 preterm infants of <2500 g birth weight [low-birth weight (LBW)] were included, and all the subjects were immunized with either PCV-7, PCV-10 or PCV-13 in this random-effects meta-analysis. For safety, the range of risk ratio (RRs) for local reaction was from 0.88 to 1.02 and from 0.94 to 1.24 for systematic reaction respectively. For immunogenicity, either post-primary or booster vaccination with PCV-7, PCV-10 or PCV-13, genomic mean concentration (GMC) of serotypes 4, 6B, 9 V, 19F and 23F was always less in preterm infants than in full-term infants, in which huge comparison of GMC was found in serotype 19F(SMD = -0.393, 95%CI:-0.612 ~ 0.175). After primary vaccination, the combined risk ratio (RRs) of immune response against seven common serotypes and additional serotype 1 was approximated to 1.00 with narrow 95 % confidence interval (CI) between preterm infants and full-term infants, and at least 91 % sero-conversion of two additional serotypes, 5 and 7F in two cohorts was observed. Furthermore, between very-low-birth-weight (VLBW) infants of <1500 g and 1501 ~ 2500 g, overall RRs of immune response to PCV-7 administration was 0.98 (95%CI: 0.96 ~ 1.00).Conclusions: Preterm infants have a great tolerance to PCV-7, PCV-10 or PCV-13 vaccination. PCV-7 could elicit optimal immune response post vaccination in preterm infants, even in VLBW infants. [ABSTRACT FROM AUTHOR]

Two new chalcones, podocarchalcones A and B ( 1 and 2), together with five known chalcones ( 3-7), were isolated from the whole plants of Desmodium podocarpum. All of their structures were determined by spectroscopic methods including 1D and 2D NMR. Compounds 1-7 were evaluated for their anti-tobacco mosaic virus (anti-TMV) activity, and they exhibited activity with inhibition rates in the range of 15.2-22.4%, respectively. [ABSTRACT FROM AUTHOR]

The human chemokine receptor CCRL2 is a member of the atypical chemokine receptor family. CCRL2 is unable to couple with G-proteins and fails to induce classical chemokine signaling for the highly conserved DRYLAIV motif essential for signaling has been changed to QRYLVFL. We investigated whether CCRL2 is involved in the chemotaxis, invasion, and proliferation of human breast cancer cells. Firstly, expression of CCRL2 was determined in six breast cancer cell lines by real-time RT-PCR and Western blot. Then, we established stable cell lines overexpressing CCRL2 to explore the function of CCRL2 in chemotaxis and invasion by transwell assays, and the signaling downstream was further investigated. The effect of CCRL2 on proliferation was detected by colony formation assays and tumor xenograft study. We found that stable overexpression of CCRL2 in MDA-MB-231 and BT-549 cells attenuated the chemotaxis and invasion stimulated by its ligand CCL2. CCRL2 inhibits p38 MAPK (p38) phosphorylation and up-regulates the expression of E-cadherin. This effect was eliminated by the inhibitor of p38 MAPK. CCRL2 inhibited the growth of breast cancer cells in vitro and in vivo. Our results suggest that CCRL2 functions as a tumor suppressor in human breast cancer cells. [ABSTRACT FROM AUTHOR]

Reactive oxygen species (ROS) and antioxidant ingredients are a series of crucial signaling molecules in oxidative stress response. Under some pathological conditions such as traumatic brain injury, ischemia/reperfusion, and hypoxia in tumor, the relative excessive accumulation of ROS could break cellular homeostasis, resulting in oxidative stress and mitochondrial dysfunction. Meanwhile, autophagy is also induced. In this process, oxidative stress could promote the formation of autophagy. Autophagy, in turn, may contribute to reduce oxidative damages by engulfing and degradating oxidized substance. This short review summarizes these interactions between ROS and autophagy in related pathological conditions referred to as above with a focus on discussing internal regulatory mechanisms. The tight interactions between ROS and autophagy reflected in two aspects: the induction of autophagy by oxidative stress and the reduction of ROS by autophagy. The internal regulatory mechanisms of autophagy by ROS can be summarized as transcriptional and post-transcriptional regulation, which includes various molecular signal pathways such as ROS-FOXO3-LC3/BNIP3-autophagy, ROS-NRF2-P62-autophagy, ROS-HIF1-BNIP3/NIX-autophagy, and ROS-TIGAR-autophagy. Autophagy also may regulate ROS levels through several pathways such as chaperone-mediated autophagy pathway, mitophagy pathway, and P62 delivery pathway, which might provide a further theoretical basis for the pathogenesis of the related diseases and still need further research. [ABSTRACT FROM AUTHOR]

Hypoxia is one of severe cellular stress and it is well known to be associated with a worse outcome since a lack of oxygen accelerates the induction of apoptosis. Autophagy, an important and evolutionarily conserved mechanism for maintaining cellular homeostasis, is closely related to the apoptosis caused by hypoxia. Generally autophagy blocks the induction of apoptosis and inhibits the activation of apoptosis-associated caspase which could reduce cellular injury. However, in special cases, autophagy or autophagy-relevant proteins may help to induce apoptosis, which could aggravate cell damage under hypoxia condition. In addition, the activation of apoptosis-related proteins-caspase can also degrade autophagy-related proteins, such as Atg3, Atg4, Beclin1 protein, inhibiting autophagy. Although the relationship between autophagy and apoptosis has been known for rather complex for more than a decade, the underlying regulatory mechanisms have not been clearly understood. This short review discusses and summarizes the dual role of autophagy and the interaction and molecular regulatory mechanisms between autophagy and apoptosis under hypoxia. [ABSTRACT FROM AUTHOR]

In the present study, the formation of the wing-tip vortex from a rectangular NACA0015 wing with a square tip at the Reynolds number of 1.8×10 5 and the angles of attack (AOA) α = 8 o and 10 o were simulated with an incompressible detached eddy simulation (DES) method and the Reynolds averaged Navier-Stokes (RANS) equations with the SA model respectively. Numerical results were compared with experimental results to validate the capability of the employed methods in resolving tip vortex flows. The results show that DES model could capture the complicated three-dimensional structures in the vortex, and the streamwise vorticity and the cross-flow velocity agree with the experiment results quite well, but RANS-SA model with the same grid as that of DES failed to capture the correct structures and under-predicted the streamwise vorticity in the vortex by 40%. The present study suggests that under the same calculation cost, DES but not RANS-SA could be used to effectively predict the flow characteristics in tip vortex. [ABSTRACT FROM AUTHOR]

The expression profile in the mouse hepatitis B virus X (HBx)-transfected model was investigated in order to lay a foundation for further study on the implication of cytokines expression in hepatitis B virus (HBV) infection. Hydrodynamic injection method via the tail vein was used to establish the animal HBx-transfected model. By using microassay, the differential expression of gene in each group was analyzed, which was further confirmed by using real-time PCR and semi-quantitative PCR. Most of chemokine genes such as Ccl2, Ccl5, Ccl9, MIG and IP-10 were up-regulated in the HBx-transfected mouse model versus the control mice, which was coincided with the microarray results. Western blotting and immunohistochemistry were applied to detect the expression of MIG and IP-10 in the liver tissues. Simultaneously, ELISA was adopted to measure the content of IFN-γ in the liver tissues. DNA microassay revealed that the expression of 611 genes changed in HBx-transfected mice as compared with that in pCMV-tag2B-transfected mice, and most of the screened chemokines were up-regulated (including MIG and IP-10). Additionally, IFN-γ protein levels were increased by 20.7% ( P<0.05) in pCMV-tag2B-HBx-transfected mice as compared with the untreated mice. IFN-γ protein levels were reduced by 53.9% ( P<0.05) in pCMV-tag2B-transfected mice as compared with the untreated mice, which was consistent with the up-regulation of MIG and IP-10. It was suggested HBx transfection could induce the expression of MIG and IP-10 in the liver tissues, which might play the roles in HBV-related liver immunity and cytokines-mediated antiviral effect. [ABSTRACT FROM AUTHOR]

Transferrin receptor (TfR) has been used as a target for the antibody-based therapy of cancer due to its higher expression in tumors relative to normal tissues. Great potential has been shown by anti-TfR antibodies combined with chemotherapeutic drugs as a possible cancer therapeutic strategy. In our study, we investigated the anti-tumor effects of anti-TfR monoclonal antibody (mAb) alone or in combination with sinomenine hydrochloride in vitro. Results suggested that anti-TfR mAb or sinomenine hydrochloride could induce apoptosis, inhibit proliferation, and affect the cell cycle. A synergistic effect was found in relation to tumor growth inhibition and the induction of apoptosis when anti-TfR mAb and sinomenine hydrochloride were used simultaneously. The expression of COX-2 and VEGF protein in HepG2 cells treated with anti-TfR mAb alone was increased in line with increasing dosage of the agent. In contrast, COX-2 expression was dramatically decreased in HepG2 cells treated with sinomenine hydrochloride alone. Furthermore, we demonstrated that the inhibitory effects of sinomenine hydrochloride and anti-TfR mAb administered in combination were more prominent than when the agents were administered singly. To sum up, these results showed that the combined use of sinomenine hydrochloride and anti-TfR mAb may exert synergistic inhibitory effects on human hepatoma HepG2 cells in a COX-2-dependent manner. This finding provides new insight into how tumor cells overcome the interference of iron intake to survive and forms the basis of a new therapeutic strategy involving the development of anti-TfR mAb combined with sinomenine hydrochloride for liver cancer. [ABSTRACT FROM AUTHOR]

Purpose: The difference between combinational and pre-planned sequential therapies using regimens that include non-anthracycline and taxane in the first-line setting remains unclear. The purpose of this study is to explore the interaction between vinorelbine (N) and capecitabine (X) in breast cancer cells and to compare the simultaneous or sequential administration of the two drugs in patients with metastatic breast cancer (MBC) as first-line treatment. Methods: First, we explored the effects of vinorelbine on thymidine phosphorylase (TP) and thymidylate synthase (TS) expression in breast cancer cells. Next, we designed a prospective randomized phase II trial of MBC patients comparing the combinational and pre-planned sequential administration of vinorelbine and capecitabine in the first-line metastatic setting. The primary end point was progression-free survival (PFS). The correlation between clinical characteristics and class III β-tubulin expression and patient survival was also explored. Results: Vinorelbine upregulates TP and downregulates TS in breast cancer cells, thereby further sensitizing tumor cells to capecitabine, which indicated the proper order for sequential therapy should be N → X. Sixty patients were eligible for the phase II trial. No significant difference was observed between the combinational arm and the sequential arm in terms of progression-free survival (PFS), overall response rate (ORR), and overall survival (OS). Only in the subgroup of patients with liver metastases were median PFS and OS significantly prolonged in the combinational arm (8.5 vs. 6.4 months, P = 0.041 and 23.8 vs. 13.9 months, P = 0.028, respectively). No association between class III β-tubulin expression and patient outcome was identified. Grade 3/4 adverse events were more common in the combinational arm. Conclusions: Both the NX regimen and pre-planned sequential N → X regimen are acceptable as first-line treatments with comparable efficacies for MBC patients previously treated with anthracyclines and/or taxanes. Sequential monotherapies are recommended as the preferred approach to first-line chemotherapy for most MBC patients in the absence of an imminent visceral crisis and the need for rapid symptom and/or disease control. [ABSTRACT FROM AUTHOR]

Published data on the association between methylenetetrahydrofolate reductase gene (MTHFR) A1298C polymorphism and breast cancer risk are inconclusive. To derive a more precise estimation of the relationship, a meta-analysis was performed. Medline, PubMed, Embase, and Web of Science were searched. Crude ORs with 95% CIs were used to assess the strength of association between the MTHFR A1298C polymorphism and breast cancer risk. The pooled ORs were performed for co-dominant model (AC vs. AA, CC vs. AA), dominant model (CC + AC vs. AA), and recessive model (CC vs. AC + AA), respectively. A total of 26 studies including 12,244 cases and 15,873 controls were involved in this meta-analysis. Overall, no significant associations were found between MTHFR A1298C polymorphism and breast cancer risk when all studies pooled into the meta-analysis (AC vs. AA: OR = 0.99, 95% CI 0.94-1.05; CC vs. AA: OR 0.99, 95% CI 0.90-1.09; dominant model: OR = 0.99, 95% CI 0.95-1.04; and recessive model: OR = 0.98, 95% CI 0.90-1.08). In the subgroup analysis by ethnicity or study design, still no significant associations were found for all comparison models. In conclusion, this meta-analysis suggests that the MTHFR A1298C polymorphism may be not associated with breast cancer development. However, large sample and representative population-based studies with homogeneous breast cancer patients and well matched controls are warranted to confirm this finding. [ABSTRACT FROM AUTHOR]

Published data on the association between p21 Ser31Arg polymorphism and breast cancer risk are inconclusive. To derive a more precise estimation of the relationship, a meta-analysis was performed. Crude ORs with 95% CIs were used to assess the strength of association between the p21 Ser31Arg polymorphism and breast cancer risk. The pooled ORs were performed for co-dominant model (Ser/Arg vs. Ser/Ser, Arg/Arg vs. Ser/Ser), dominant model (Arg/Arg + Ser/Arg vs. Ser/Ser), and recessive model (Arg/Arg vs. Ser/Arg + Ser/Ser). A total of 21 studies including 22,109 cases and 29,127 controls were involved in this meta-analysis. Overall, no significant associations were found between p21 Ser31Arg polymorphism and breast cancer risk when all studies pooled into the meta-analysis. In the subgroup analysis by ethnicity, significantly increased risk was found for Caucasians (Arg/Arg vs. Ser/Ser: OR 1.496, 95% CI 1.164-1.924; and recessive model: OR 1.492, 95% CI 1.161-1.919). When stratified by study design, statistically significantly elevated risk was found for population-based studies (Ser/Arg vs. Ser/Ser: OR 1.085, 95% CI 1.019-1.156). In conclusion, this meta-analysis suggests that the p21 Ser31Arg polymorphism may be associated with breast cancer development in Caucasian. However, large sample and representative population-based studies with homogeneous breast cancer patients and well-matched controls are warranted to confirm this finding. [ABSTRACT FROM AUTHOR]

This paper reports the numerical research of tunnel hood effects on high speed train-tunnel compression wave. The three-dimensional simulation with real geometry is carried out by the implementation of a commercial computational code. The train speed is 350 km/h. The train/tunnel blockage ratio is 0.115. Nine different types of tunnel hoods were studied. The calculation results showed that the hood length, the hood cross sectional area and the ventilation holes might have significant influence on the first compression wave, and inclined entry or asymmetric distribution of the ventilation holes is not available for alleviating the impulsive wave. [ABSTRACT FROM AUTHOR]

Purpose: 1,1-Bis(3-indolyl)-1-(p-substituted phenyl)methanes (C-DIMs) substituted in the phenyl ring with a para-, t-butyl, trifluoromethyl (DIM-C-pPhCF(3)) or phenyl (DIM-C-pPhC(6)H(5)) group activate peroxisome proliferator-activated receptor gamma (PPARgamma) in several cancer cell lines, and DIM-C-pPhCF(3) also activates the orphan receptor Nur77. In this study, we have examined the effects of 5,5'-dihydroxy, 5,5'-dimethyl, 5,5'-dibromo, 5,5'-dinitro and 5,5'-dimethoxyindole ring-substituted analogs of DIM-C-pPhC(6)H(5) on their activity as PPARgamma agonists.Methods: Various substituted C-DIM analogs were used to investigate their growth-inhibitory activities and activation of PPARgamma-mediated transactivation in colon and pancreatic cancer cells. Their structure-dependent induction of putative PPARgamma-responsive genes/proteins including p21, KLF-4 and caveolin1 were also determined by Western and Northern blot analysis.Results: Introduction of the 5,5'-dihydroxy and 5,5'-dimethyl substituents enhanced activation of PPARgamma in colon and pancreatic cancer cells. However, activation of p21 in Panc28 pancreatic cancer cells and induction of caveolin-1 and KLF4 in colon cancer cells by the C-DIM compounds were structure- and cell context-dependent.Conclusions: The results demonstrate that DIM-C-pPhC(6)H(5) and indole ring-substituted analogs are selective PPARgamma modulators. [ABSTRACT FROM AUTHOR]

Numerical investigation was conducted on an airship of hull-fin configuration for aerodynamic and aeroelastic characteristics in three-dimensional viscous flows. The mathematical model was built and the corresponding numerical code was developed for the fluid-structure interaction problem. The governing equations of the viscous flow with LL-Low Reynolds modified model were solved by the standard SIMPLE algorithm based on the finite volume method. A fluid-structure coupled method was employed to solve the nonlinear aeroelasticity problem for the airship. The computational results of the viscous flow are in good agreement with the experimental measurements. The simulation on the aeroelastic behavior of the airship in a trimmed flight reveals the effect of structure flexibility on the aerodynamic performance. [ABSTRACT FROM AUTHOR]

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The purpose of this study was to construct expression vectors of idiotype (Id) SmIg in patients with B-chronic lymphocytic leukemia and to express them in E.coli to obtain recombinant Id, and to investigate the effect of the protein on the proliferation and secretion of IL-2 and IFN-γ of stimulated peripheral blood mononuclear cells (PBMC) in vitro. Light chain gene and Fd fragment of heavy chain gene were inserted into fd-tet-DOG2 vector to construct fd-tet-DOG2-Fab. Fab gene was further cloned into expression vector pHEN2 to construct the soluble expression vector pHEN2-Fab. After induction by IPTG, Fab protein was purified by Ni-NTA-chromatography. MTT was used to determine the effects of purified protein on the proliferation of stimulated PBMC in vitro and the concentrations of IL-2 and IFN-γ in the culture supernatants were detected by ELISA. The results showed that recombinant pHEN2-Fab expression vector was constructed successfully. Fab protein was expressed in positive clone after induced by IPTG and two specific bands at 24–25 kD position were observed by SDS-PAGE electrophoresis. Proliferation of PBMC could be induced by purified Fab and the concentrations of IL-2 and IFN-γ in culture supernatants were increased significantly after induction. It was suggested that the expression vector of SmIg Fab fragment was constructed successfully, and expressed and secreted from E. coli. The Fab protein could induce proliferation of PBMC and promote secretion of IL-2 and IFN-γ. [ABSTRACT FROM AUTHOR]

An investigation of the ventilated supercavitation for a supercavitating vehicle pitching up and down in the supercavity was carried out in a high-speed water tunnel. The emphasis is laid on the understanding of the interaction of the vehicle aft body with the cavity boundary. The flow characteristics were measured and the stability of supercaviting flow with different pitching frequencies and amplitudes was analyzed. In particular, the objectives of this study are to understand the effect of the impact upon the cavity distortion, and to quantify the impact process by investigating the evolution of the pressure inside the cavity and then the loads on the vehicle during the pitching motion. It is also shown that the evolution of the pressure detected in different,as inside the supercavity, is coherent and uniform during the periods of the pitching motion. This study is of direct relevance to reliable and accurate prediction of hydrodynamic loads associated with the slamming and impact on supercavitating vehicles. [ABSTRACT FROM AUTHOR]

Due to the flexibility of the envelope of large stratosphere airships, the aerodynamic solution of such airship is closely related to its shape and the external aerodynamic forces which lead to the structural deformation. It is essentially one of the Fluid-Structure Interaction (FSI) problems. This article aims at the numerical investigation of nonlinear airship aeroelasticity in consideration of aerodynamics and structure coupling, using an iteration method. The three-dimensional flow around the airship was numerically studied by means of the SIMPLE method based on the finite volume method. Nonlinear finite element analysis was employed for geometrically nonlinear deformation of the airship shape. Comparison of aerodynamic parameters and the pressure distribution between rigid and aeroelastic models was conducted when an airship is in a trimmed flight state in specified flight conditions. The effect of aeroelasticity on the airship aerodynamics was detailed. [ABSTRACT FROM AUTHOR]

The effects of survivin antisense RNA on proliferation of leukemia cell line HL-60 and taxol-induced chemotherapy was explored. A cDNA fragment of survivin obtained by RT-PCR was inserted into a plamid vector named pcDNA3 in the reverse direction. The vector encoding antisense RNA of survivin was confirmed by restriction enzyme digestion and DNA sequencing. The recombinant plasmid was delivered into HL-60 cells by electroporation. Growth curves were plotted based on cell counting. Trypan blue dye exclusion assay and MTT assay were carried out after the cells were incubated with taxol. DNA gel electrophoresis and nuclear staining were performed for cell apoptosis assay. The correct construction of the recombinant plasmid has been identified by restriction enzyme digestion and DNA sequencing. A stable down-regulation has been achieved in HL-60 SVVas cells after G418 selection. Compared to HL-60 cells, the proliferation of HL-60 SVVas cells was significantly inhibited ( P<0.05). Cytotoxicity assays indicated that IC50 of HL-60 SVVas for taxol was relatively lower than controls ( P<0.01). Apoptosis assays revealed that taxol-induced apoptosis was detected in HL-60 SVVas cells incubated with 50 ng/ml taxol for 12 h, while in HL-60 cells incubated with 100 ng/ml taxol for 72 h. It was suggested that Survivin antisense RNA could inhibit the proliferation of HL-60 cells and enhance taxol-induced apoptosis in HL-60 cells, which may lay an experimental foundation for further research on gene therapy in leukemia. [ABSTRACT FROM AUTHOR]