Data_Sheet_2_Detecting apathy in patients with cerebral small vessel disease.docx

BackgroundApathy is attracting more and more attention in clinical practice. As one of the most common features of cerebral small vessel disease (CSVD), the assessment of apathy still mainly relies on observers. With the development of Information and Communication Technologies (ICTs), new objective tools take part in the early detection of apathy.ObjectivesTo detect apathy in patients with CSVD and find out the relationship between apathy and actigraphic data sampled from the diurnal and nocturnal periods.MethodsA total of 56 patients with CSVD were recruited for a cross-sectional observational study. Apathy was diagnosed by the diagnostic criteria for apathy in neurocognitive disorders. The presence of lacunes, white matter hyperintensities, cerebral microbleeds (CMBs), and perivascular spaces (PVS) in magnetic resonance imaging (MRI) images were rated independently. Actigraph devices were worn in the non-dominant hands of each subject for 7 consecutive days to collect samples of raw data, and diurnal vector magnitude (VM) and a series of sleep quality variables were obtained.ResultsWe found that the frequency of apathy in Chinese patients with CSVD reached 37.50%. Patients in the Apathy+ group showed more lacunes and CMBs, and higher Fazekas scores in comparison to apathy-group individuals. Diurnal VM, instead of other sleep quality variables, was lower in CSVD patients with apathy relative to those without apathy. Lastly, we discovered that diurnal VM and total time in bed (TTB) correlated negatively with apathy severity in patients with CSVD.ConclusionActigraphy is a promising choice to evaluate apathy in patients with CSVD.</p

Schizandrin A exerts anti-tumor effects on A375 cells by down-regulating H19

Malignant melanoma (MM) is one of the malignant tumors with highly metastatic and aggressive biological actions. Schizandrin A (SchA) is a bioactive lignin compound with strong anti-oxidant and anti-aging properties, which is stable at room temperature and is often stored in a cool dry place. Hence, we investigated the effects of SchA on MM cell line A375 and its underlying mechanism. A375 cells were used to construct an in vitro MM cell model. Cell viability, proliferation, apoptosis, and migration were detected by Cell Counting Kit-8, BrdU assay, flow cytometry, and transwell two-chamber assay, respectively. The cell cycle-related protein cyclin D1 and cell apoptotic proteins (Bcl-2, Bax, cleaved-caspase-3, and cleaved-caspase-9) were analyzed by western blot. Alteration of H19 expression was achieved by transfecting with pEX-H19. PI3K/AKT pathway was measured by detecting phosphorylation of PI3K and AKT. SchA significantly decreased cell viability in a dose-dependent manner. Furthermore, SchA inhibited cell proliferation and cyclin D1 expression. SchA increased cell apoptosis along with the up-regulation of pro-apoptotic proteins (cleaved-caspase-3, cleaved-caspase-9, and Bax) and the down-regulation of anti-apoptotic protein (Bcl-2). Besides, SchA decreased migration and down-regulated matrix metalloproteinases (MMP)-2 and MMP-9. SchA down-regulated lncRNA H19. Overexpression of H19 blockaded the inhibitory effects of SchA on A375 cells. SchA decreased the phosphorylation of PI3K and AKT while H19 overexpression promoted the phosphorylation of PI3K and AKT. SchA inhibited A375 cell growth, migration, and the PI3K/AKT pathway through down-regulating H19.</div

Data_Sheet_1_Detecting apathy in patients with cerebral small vessel disease.docx

BackgroundApathy is attracting more and more attention in clinical practice. As one of the most common features of cerebral small vessel disease (CSVD), the assessment of apathy still mainly relies on observers. With the development of Information and Communication Technologies (ICTs), new objective tools take part in the early detection of apathy.ObjectivesTo detect apathy in patients with CSVD and find out the relationship between apathy and actigraphic data sampled from the diurnal and nocturnal periods.MethodsA total of 56 patients with CSVD were recruited for a cross-sectional observational study. Apathy was diagnosed by the diagnostic criteria for apathy in neurocognitive disorders. The presence of lacunes, white matter hyperintensities, cerebral microbleeds (CMBs), and perivascular spaces (PVS) in magnetic resonance imaging (MRI) images were rated independently. Actigraph devices were worn in the non-dominant hands of each subject for 7 consecutive days to collect samples of raw data, and diurnal vector magnitude (VM) and a series of sleep quality variables were obtained.ResultsWe found that the frequency of apathy in Chinese patients with CSVD reached 37.50%. Patients in the Apathy+ group showed more lacunes and CMBs, and higher Fazekas scores in comparison to apathy-group individuals. Diurnal VM, instead of other sleep quality variables, was lower in CSVD patients with apathy relative to those without apathy. Lastly, we discovered that diurnal VM and total time in bed (TTB) correlated negatively with apathy severity in patients with CSVD.ConclusionActigraphy is a promising choice to evaluate apathy in patients with CSVD.</p

Luteolin suppresses lung cancer progression through targeting the circ_0000190/miR-130a-3p/notch-1 signaling pathway

Lung cancer is the leading cause of cancer mortality worldwide. Luteolin has been reported to repress the development of lung cancer. And circular RNAs (circRNAs) circ_0000190 was upregulated in lung cancer tissues. This study is designed to explore the roles of luteolin and circ_0000190 in lung cancer progression. Cell viability, colony number, migration, invasion, and apoptosis were detected by Cell Counting Kit-8 (CCK-8), colony formation, transwell, and flow cytometry assays, severally. The lactate dehydrogenase (LDH) release was determined by special kits. Protein levels of B-celllymphoma-2 (Bcl-2) Cleaved-caspase3 (casp3), Bcl-2 related X protein (Bax), Notch-1, hairy enhance of split-1(Hes-1), and vascular endothelium growth factor (VEGF) were determined by western blot assay. Circ_0000190 andmicroRNA-130a-3p (miR-130a-3p) expression were measured by real-time quantitative polymerase chain reaction (RT-qPCR). The binding relationship between circ_0000190 andmiR-130a-3pwas predicted by starbase and then verified by a dual-luciferase reporter and RNA pull-down assays. The biological roles of Luteolin and circ_0000190 on tumor growth of lung cancer were examined by the xenograft tumor model in vivo. Luteolin inhibited cell viability, colony formation, migration, invasion, and promoted apoptosis of lung cancer cells. Moreover, overexpression of circ_0000190 could counteract the suppression role of luteolin on lung cancer development. Andcirc_0000190 directly bound with miR-130a-3p. Luteolin blocked lung cancer cell growth, metastasis, and Notch-1 signaling pathway by modulating the circ_0000190/miR-130a-3pin vitro. Luteolin repressed tumor growth of lung cancer in vivo by regulating circ_0000190. Luteolin dampened the progression of lung cancer partly by regulating circ_0000190/miR-130a-3p, providing an underlying therapeutic target for lung cancer.</p

Rapid Preparation of Porous Ni–Al Intermetallics by Thermal Explosion

Porous Ni3Al, NiAl, and NiAl3 intermetallics have been synthesized through simple and rapid process of thermal explosion (TE) from 75 at.% Ni/25 at.% Al, 50 at.% Ni/50 at.% Al and 25 at.% Ni/75 at.% Al elemental powders. The effect of the three components on temperature profile, phase composition, pore structure, and oxidation resistance were investigated. The results showed that the temperature of the specimens increased rapidly from 638°C to 1381°C, 620°C to 1613°C and 642°C to 1172°C in a few seconds. X-ray diffraction patterns indicated that Ni3Al, NiAl, and NiAl3 were the main phase or single-phase compounds in the TE products. Porous Ni3Al, NiAl, and NiAl3 intermetallics showed variable pore structures. Moreover, all the products of three components exhibited good oxidation resistance, particularly the porous NiAl and NiAl3 intermetallics.</p

The effect of Fe in the rapid thermal explosion synthesis and the high-temperature corrosion behavior of porous Co-Al-Fe intermetallic

High porosity Co-Al-Fe intermetallic with 3D-microstructures were one-step synthesized via a novel thermal explosion reaction. A link between pore structure and permeability was established using 3D-XRM technology. The corrosion resistance of the samples with different Fe contents was investigated at 900 °C under an oxygen/sulphur atmosphere for up to 120 h. The results showed that the pore structure of the samples remains stable, and the internal matrices are intact due to the formation of a thin protective layer of Al2O3 and Fe2O3 on the surface of the product skeleton. In addition, inward diffusion of S leads to the formation of FeS nodules

Data_Sheet_1_Serum Amyloid A Stimulates Vascular and Renal Dysfunction in Apolipoprotein E-Deficient Mice Fed a Normal Chow Diet.pdf

Elevated serum amyloid A (SAA) levels may promote endothelial dysfunction, which is linked to cardiovascular and renal pathologies. We investigated the effect of SAA on vascular and renal function in apolipoprotein E-deficient (ApoE−/−) mice. Male ApoE−/− mice received vehicle (control), low-level lipopolysaccharide (LPS), or recombinant human SAA by i.p. injection every third day for 2 weeks. Heart, aorta and kidney were harvested between 3 days and 18 weeks after treatment. SAA administration increased vascular cell adhesion molecule (VCAM)-1 expression and circulating monocyte chemotactic protein (MCP)-1 and decreased aortic cyclic guanosine monophosphate (cGMP), consistent with SAA inhibiting nitric oxide bioactivity. In addition, binding of labeled leukocytes to excised aorta increased as monitored using an ex vivo leukocyte adhesion assay. Renal injury was evident 4 weeks after commencement of SAA treatment, manifesting as increased plasma urea, urinary protein, oxidized lipids, urinary kidney injury molecule (KIM)-1 and multiple cytokines and chemokines in kidney tissue, relative to controls. Phosphorylation of nuclear-factor-kappa-beta (NFκB-p-P65), tissue factor (TF), and macrophage recruitment increased in kidneys from ApoE−/− mice 4 weeks after SAA treatment, confirming that SAA elicited a pro-inflammatory and pro-thrombotic phenotype. These data indicate that SAA impairs endothelial and renal function in ApoE−/− mice in the absence of a high-fat diet.</p