Dynamic Simulation of Deposition Processes of Spacecraft Molecular Contamination

Accurate simulation and calculation of the deposition of outgassing molecule can shorten the cycle and reduce the cost of vacuum tests on satellites. It also provides a reference for contamination protection design by systems engineers. In this study, the molecular outgassing, transport and deposition processes were simulated by diffusion theory, the angle coefficient method, and the first-order desorption equation, respectively. The simulation results were consistent with the test data trends, but deviated from the test values. Given the effect of initial molecular outgassing rate, diffusion coefficient and residence time on the deposition mass, it was surmised that considering the molecular species and the weight mass rate would improve the calculation result. These considerations indeed improved the numerical simulations of high-vacuum contamination

Interleukin-11 Promotes the Progress of Gastric Carcinoma via Abnormally Expressed Versican

Versican, a ubiquitous component of the extracellular matrix (ECM), accumulates both in tumor stroma and cancer cells and is highly regulated by various cytokines. The aberrant expression of versican and its isoforms is known to modulate cell proliferation, differentiation, and migration, all of which are features of the invasion and metastasis of cancer; versican is also known to favour the homeostasis of the ECM. Interleukin-11 (IL-11) is an important cytokine that exhibits a wide variety of biological effects in gastric cancer development. Here, we analysed the expression of versican isoforms and found that the major isoforms expressed by both gastric carcinoma tissue and gastric cell lines were V0 and V1, and V1 was significantly higher in gastric carcinoma tissue. The treatment of the gastric cell lines AGS and MKN45 with rhIL-11 resulted in a significant increase in the expression of V0 and V1. Exogenous IL-11 increased migration in AGS and MKN45 cells, whereas these effects were reversed when the expression of V0 and V1 were abolished by siRNA targeting versican V0/V1. Collectively, these findings suggest that the abnormally expressed versican and its isoforms participate, at least in part, in the progress of gastric carcinoma triggered by IL-11

Associations between microstructural tissue changes, white matter hyperintensity severity, and cognitive impairment: an intravoxel incoherent motion imaging study

IntroductionWhite matter hyperintensities (WMHs) are a common age- and vascular risk factor-related disease and have been recognized to play an important role in cognitive impairment. However, it is still unclear what the mechanism of this effect is. In this study, intravoxel incoherent motion (IVIM) was employed to assess the microvasculature and parenchymal microstructure changes of WMHs and explore their relationship with cognitive function.MethodsForty-nine WMH patients and thirty-one healthy controls underwent IVIM imaging, a diffusion technique that provides parenchymal diffusivity D, intravascular diffusivity D*, and perfusion fraction f . The IVIM dual exponential model parameters were obtained in specific regions of interest, including deep white matter hyperintensities (DWMHs), periventricular white matter hyperintensities (PWMHs), and normal-appearing white matter (NAWM). The independent-sample t-test or Mann–Whitney U-test was utilized to compare IVIM parameters between patients and controls. The Kruskal–Wallis test or one-way analysis of variance was used to compare IVIM parameters among DWMH, PWMH, and NAWM for patients. The Wilcoxon two-sample test or independent-sample t-test was used to assess the differences in IVIM parameters based on the severity of WMH. The multivariate linear regression analysis was conducted to explore the factors influencing cognitive scores.ResultsWMH patients exhibited significantly higher parenchymal diffusivity D than controls in DWMH, PWMH, and NAWM (all p < 0.05). IVIM parameters in the three groups (DWMH, PWMH, and NAWM) were significantly different for patients (all p < 0.001). The severe WMH group had a significantly higher parenchymal diffusivity D (DWMH and PWMH) than mild WMH (both p < 0.05). The multiple linear regression analysis identified D in DWMH and PWMH as influencing cognitive function scores (all p < 0.05).ConclusionIVIM has the potential to provide a quantitative marker of parenchymal diffusivity for assessing the severity of WMH and may serve as a quantitative marker of cognitive dysfunction in WMH patients

Diffusion basis spectrum imaging measures anti-inflammatory and neuroprotective effects of fingolimod on murine optic neuritis

OBJECTIVE: To prospectively determine whether diffusion basis spectrum imaging (DBSI) detects, differentiates and quantitates coexisting inflammation, demyelination, axonal injury and axon loss in mice with optic neuritis (ON) due to experimental autoimmune encephalomyelitis (EAE), and to determine if DBSI accurately measures effects of fingolimod on underlying pathology. METHODS: EAE was induced in 7-week-old C57BL/6 female mice. Visual acuity (VA) was assessed daily to detect onset of ON after which daily oral-treatment with either fingolimod (1 mg/kg) or saline was given for ten weeks. In vivo DBSI scans of optic nerves were performed at baseline, 2-, 6- and 10-weeks post treatment. DBSI-derived metrics including restricted isotropic diffusion tensor fraction (putatively reflecting cellularity), non-restricted isotropic diffusion tensor fraction (putatively reflecting vasogenic edema), DBSI-derived axonal volume, axial diffusivity, λ RESULTS: Optic nerves of fingolimod-treated mice exhibited significantly better (p \u3c 0.05) VA than saline-treated group at each time point. During ten-week of treatment, DBSI-derived non-restricted and restricted-isotropic-diffusion-tensor fractions, and axonal volumes were not significantly different (p \u3e 0.05) from the baseline values in fingolimod-treated mice. Transient DBSI-λ CONCLUSION: DBSI was used to assess changes of the underlying optic nerve pathologies in EAE mice with ON, exhibiting great potential as a noninvasive outcome measure for monitoring disease progression and therapeutic efficacy for MS

The value of coordinated analysis of multimodal atherosclerotic plaque imaging in the assessment of cardiovascular and cerebrovascular events

BackgroundAlthough atherosclerosis (AS) can affect multiple vascular beds, previous studies have focused on the analysis of single-site AS plaques.ObjectiveThe aim of this study is to explore the differences or similarities in the characteristics of atherosclerotic plaque found in the internal carotid artery, cerebral artery, and coronary artery between patients with atherosclerotic cardiovascular disease (ASCVD) and those without events.MethodsPatients aged ≥ 18 years who underwent both high-resolution vessel wall imaging (HR-VWI) and coronary computed tomography angiography (CCTA) were retrospectively collected and categorized into the ASCVD group and the non-event group. The plaques were then categorized into culprit plaques, non-culprit plaques, and non-event plaques. Plaque morphological data such as stenosis, stenosis grades, plaque length (PL), plaque volume (PV), minimal lumen area (MLA), enhancement grade, and plaque composition data such as calcified plaque volume (CPV), fibrotic plaque volume (FPV), fibro-lipid plaque volume (FLPV), lipid plaque volume (LPV), calcified plaque volume ratio (CPR), fibrotic plaque volume ratio (FPR), fibro-lipid plaque ratio (FLPR), lipid plaque volume ratio (LPR), intraplaque hemorrhage volume (IPHV), and intraplaque hemorrhage volume ratio (IPHR)were recorded and analyzed.ResultsA total of 44 patients (mean age 66 years, SD 9 years, 28 men) were included. In cervicocephalic plaques, the ASCVD group had more severe stenosis grades (p = 0.030) and demonstrated significant differences in LPV, LPR, and CPV (p = 0.044, 0.030, 0.020) compared with the non-event group. In coronary plaques, the ASCVD group had plaques with greater stenosis (p < 0.001), more severe stenosis grades (p < 0.001), larger volumes (p = 0.001), longer length (p = 0.008), larger FLPV (p = 0.012), larger FPV (p = 0.002), and higher FPR (p = 0.043) compared with the non-event group. There were significant differences observed in stenosis (HR-VWI, CCTA: p < 0.001, p < 0.001), stenosis grades (HR-VWI, CCTA: p < 0.001, p < 0.001), plaque length (HR-VWI, CCTA: p = 0.028, p < 0.001), and plaque volume (HR-VWI, CCTA: p = 0.013, p = 0.018) between the non-event plaque, non-culprit plaque, and culprit plaque. In the image analysis of HR-VWI, there were differences observed between IPHR (p < 0.001), LPR (p = 0.001), FPV (p = 0.011), and CPV (p = 0.015) among the three groups of plaques. FLPV and FPV were significantly different among the three different plaque types from the coronary artery (p = 0.043, p = 0.022).ConclusionThere is a consistent pattern of change in plaque characteristics between the cervicocephalic and coronary arteries in the same patient

Down-Regulation of MiR-127 Facilitates Hepatocyte Proliferation during Rat Liver Regeneration

Liver regeneration (LR) after partial hepatectomy (PH) involves the proliferation and apoptosis of hepatocytes, and microRNAs have been shown to post-transcriptionally regulate genes involved in the regulation of these processes. To explore the role of miR-127 during LR, the expression patterns of miR-127 and its related proteins were investigated. MiR-127 was introduced into a rat liver cell line to examine its effects on the potential target genes Bcl6 and Setd8, and functional studies were undertaken. We discovered that miR-127 was down-regulated and inversely correlated with the expression of Bcl6 and Setd8 at 24 hours after PH, a time at which hypermethylation of the promoter region of the miR-127 gene was detected. Furthermore, in BRL-3A rat liver cells, we observed that overexpression of miR-127 significantly suppressed cell growth and directly inhibited the expression of Bcl6 and Setd8. The results suggest that down-regulation of miR-127 may be due to the rapid methylation of its promoter during the first 24 h after PH, and this event facilitates hepatocyte proliferation by releasing Bcl6 and Setd8. These findings support a miRNA-mediated negative regulation pattern in LR and implicate an anti-proliferative role for miR-127 in liver cells