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Objective. To analyze and predict the progress of patients with lacunar infarction by analyzing the levels of serum NO, PGI2, and Ox-LDL produced by endothelial cells. Methods. 138 patients with lacunar infarction and 34 healthy people were selected. The selected samples were divided into progressive group, nonprogressive group, and control group for biochemical test and endothelial function test. The levels of serum NO, PGI2, and Ox-LDL were obtained. The observation indexes of different groups were compared for statistical analysis and multivariate logistic regression analysis. Results. The indexes of LI patients in the nonprogression group were different from those in the control group. The content of Ox-LDL in the nonprogression group was higher than that in the control group, while the indexes of serum NO and PGI2 were lower than that in the control group. The level of Ox-LDL in LI patients in the progressive group was much higher than that in healthy people in the control group seven days after admission, while the levels of serum NO and PGI2 were lower, and the difference of serum on was more obvious. The level of Ox-LDL in the progressive group was much higher than that in the nonprogressive group, while the levels of serum NO and PGI2 in the progressive group were lower, and the level of serum NO was significantly different from that in the nonprogressive group. Ox − LDL > 76.48 U / L , NO > 55.24 ummol / L , and PGI 2 > 29.78 ng / L were independent risk factors for the progression of lacunar infarction. Conclusion. Because the patients with lacunar infarction have endothelium-dependent relaxation disorder, the changes of serum NO, PGI2, and Ox-LDL can be used as the evaluation index of the disease progress of patients with lacunar infarction and can be widely used in clinical detection.

Objective: The purpose of this paper was to study the protective effect of paeoniflorin on acute cerebral ischemia. The animal model of cerebral infarction induced by Middle Cerebral Artery Occlusion (MCAO) was blocked by the suture method. Sixty SD rats were randomly divided into the shame group, MCAO group, paeoniflorin (60, 120, 240 mg/kg, respectively) and Nimodipine (NMDP) group (n = 10 per group). Methods: The rats were intragastrically administered immediately after the operation. After 7 days of gavage, the brains were decapitated at 24 h. Hematoxylin and Eosin (HE) staining was used to observe the degree of cell damage in the cerebral cortex of rats. Immunohistochemistry was used to detect silver plating and to observe changes in nerve cells. Rats in the model group showed obvious symptoms of neurological deficits, such as the ischemic morphological changed, the Malondialdehyde (MDA), Lactate Dehydrogenase (LD) content and lactate dehydrogenase (LDH) activity were significantly increased in the ischemic brain tissue, while the Superoxide Dismutase (SOD) activity was decreased. Results: The decrease in Na+-K+-ATPase activity was significantly lower than that in the sham group. The neurological symptoms and signs of MCAO in the different doses of paeoniflorin group were improved, and the neuronal edema in the cortical area was alleviated. The activities of SOD, LDH and Na+-K+-ATPase were significantly increased, and the contents of MDA and LD were decreased. Conclusion: Therefore, paeoniflorin could alleviate the degree of tissue damage in rats with acute cerebral infarction, inhabit the formation of free radicals in the brain tissue after ischemia, and reduce the degree of lipid peroxidation. Thus, the degree of cell damage was reduced greatly and a protective effect was showed on cerebral ischemia.

Aim: This study focused on the expression pattern of long non-coding RNA maternally expressed gene 3 (MEG3) and its value in ischemic stroke (IS). Methods: The expression pattern and the roles of MEG3 in the development of IS were explored in mice IS model and human brain microvascular endothelial cells (hBMECs). A case-control study, including 215 IS patients and 153 controls, was also conducted to investigate its prognostic value. Results: In vivo study showed that MEG3 increased significantly in the IS group (P = 0.004), and its level remained stable within 3 to 48h after the onset of IS. Besides, the survival time of the mouse in the high MEG3 group was significantly lower than that in the low MEG3 group (P = 0.042). In vitro study showed that oxygen–glucose deprivation (OGD) treatment significantly up-regulated expressions of MEG3, Bax, and cleaved caspase-3, and further promoted apoptosis of hBMECs, while si-MEG3 blocked these effects. A human study showed that MEG3 increased markedly within 48h of IS onset and was positively associated with the National Institutes of Health Stroke Scale (r = 0.347, P < 0.001), modified Rankin Scale (r = 0.385, P < 0.001), high-sensitivity C-reactive protein (r = 0.221, P = 0.002) level, and infarct volume (r = 0.201, P = 0.006). Overall survival analysis showed that patients with higher MEG3 expression within 48h had a relatively poor prognosis (P < 0.001). Meanwhile, multivariate analysis revealed that MEG3 was an independent prognostic marker for unfavorable functional outcome and death in IS patients. Conclusions: This study suggested that MEG3 might be considered as an intervention point and potential prognostic indicator for IS.

Dihydromyricetin (DMY) is a natural flavonoid that possesses a wide range of pharmacological properties. The aim of the present study was to determine whether DMY could protect against nerve cell injury following ischemic stroke through antioxidant and neuroprotective effects. The effects of DMY on the viability, oxidative stress and apoptosis of HT22 cells following oxygen‑glucose deprivation and re‑oxygenation (OGD/R) were examined using MTT, lactate dehydrogenase (LDH), superoxide (SOD), malondialdehyde (MDA), western blot and TUNEL assays. Furthermore, Wnt/β‑catenin signaling proteins in OGD/R‑stimulated HT22 cells were detected in the presence or absence of DMY. In a separate experiment, the effect of DMY on OGD/R‑induced HT22 cell injury was also observed in the presence of the Wnt/β‑catenin inhibitor, XAV939. The results demonstrated that DMY had no impact on the survival of untreated HT22 cells, although DMY treatment significantly increased cell viability and inhibited cytotoxicity, oxidative stress and apoptosis following OGD/R. In addition, DMY upregulated the expression of Wnt/β‑catenin in OGD/R‑stimulated HT22 cells. In conclusion, DMY protected HT22 cells from OGD/R‑induced oxidative stress and apoptosis, and its effects may be mediated by the activation of the Wnt/β‑catenin signaling pathway.

Activated platelets (PLTs) participate in the regulation of tumor angiogenesis, and tumors can activate PLTs. Whether co-culture of lung carcinoma with PLTs improves the function of human umbilical vein endothelial cells (HUVECs) requires further investigation. The present study aimed to investigate the impact of H1975 cell crosstalk with PLTs on the proliferation, migration and tube formation of HUVECs. Following generation of cell-derived supernatants and construction of the co-culture system, Cell Counting Kit-8, flow cytometry, transmission electron microscopy and a meter for epithelial measurement were performed to detect the proliferative ability of HUVECs. Furthermore, the wound healing and Transwell migration assays were performed to detect the migratory ability of HUVECs. A tube formation assay was performed to assess angiogenesis, ELISA was applied to detect the content of vascular endothelial growth factor (VEGF) and western blotting was carried out to measure the expression levels of VEGF receptor 2 (VEGFR2) in HUVECs. Compared with single-cultured HUVECs (control), co-culture with H1975 cells and PLTs (Exp_HP) improved cell proliferation, increased the proportion of cells in the S-phase, destroyed the cell ultrastructure and decreased transepithelial electrical resistance in HUVECs. In addition, a higher relative migration rate, greater number of migrated cells, stronger tube-forming ability and increased expression of VEGF and VEGFR2 were detected in the Exp_HP group compared with the control group. The properties of HUVECs in Exp_H (co-cultured with H1975 cells) were similar to those in Exp_HP, but significantly weaker. Taken together, the results of the present study suggest that tumor cells interacting with PLTs may play an important role in tumor angiogenesis by affecting or mediating changes in the properties of vascular endothelial cells (VECs).

An intrinsic flame retardant vinyl ester TGIC-AA-DOPO constructed by phosphaphenanthrene and triazine-trione groups was successfully synthesized via the reaction between 1,3,5-triglycidyl isocyanurate (TGIC), acrylic acid and 9,10-dihydro-9-oxa-10-phosphaphenanthrene-10-oxide (DOPO). The structure of TGIC-AA-DOPO was characterized in detail by fourier transform infrared spectroscopy (FTIR), 1 H and 31 P nuclear magnetic resonance (NMR) and liquid chromatography-high resolution mass spectrometry (LC-HRMS). The intrinsic P-N-containing flame retardant vinyl ester resin (IFR-VER) was prepared after diluting TGIC-AA-DOPO with styrene (st) and triallyl isocyanurate (TAIC). The flame retardancy, thermal properties and combustion behavior of IFR-VER were respectively investigated by a series of tests involving limited oxygen index (LOI) measurement, UL-94 vertical burning test, cone calorimeter test, thermogravimetric analysis (TGA) and dynamic mechanical analysis (DMA). The results showed that the as-obtained resin system exhibited a dramatic improvement in flame retardance. In the case of 40 wt% TAIC in resin system, the LOI value achieved 31%, leading to the UL-94 V-0 rating. In addition, compared with the 901-VER, the peak heat release rate (pk-HRR), average of heat release rate (av-HRR), total heat release (THR) and average effective heat of combustion (av-EHC) of the IFR-VER containing 40% TAIC diluent were decreased by 48%, 60%, 41% and 24% respectively. The diphase flame retardant effect of the prepared IFR-VER during combustion was demonstrated by the results of Py-GC/MS, FTIR, laser raman spectroscopy and scanning electron microscope (SEM).

In this paper, poly (tetrahydrofuranyl ether diol) and trimethylolpropane (TMP) were used respectively as chain extender and cross-linking agent to fabricate polyurethane resin. The morphol...

Parkinson's disease (PD) is characterized by the loss of dopaminergic neurons in the substantia nigra and striatum. Aging is the most important risk factor of PD. Ferroptosis is an iron-dependent form of cell death associated with PD. However, it is not clear whether ferroptosis accelerates PD by promoting cellular senescence. This study investigated the mechanism of 1-methyl-4-phenylpyridinium (MPP+) -induced PC12 cells injury. We found that MPP+ induced cell senescence with increased β-galactosidase activity and the expression of p53, p21 and p16 activation in cells. In addition, MPP+ treatment showed smaller mitochondria and increased membrane density, downregulation of ferritin heavy chain 1 expression and upregulation of acyl-CoA synthetase long chain family member 4 expression, and enhanced levels of oxidative stress, which were important characteristics of ferroptosis. Ferrostatin-1 (Fer-1), a ferroptosis inhibitor, was tested to eliminate MPP+-induced cell senescence. Fer-1 downregulated the expression of p53 and upregulated the expression of solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase-4 (GPX4) in MPP+-induced ferroptosis. Inhibition of p53 eliminated cell senescence by upregulation the expression of of SLC7A11 and GPX4. Thus, these results suggest that MPP+ induces senescence in PC12 cells via the p53/ SLC7A11/ GPX4 signaling pathway in the ferroptosis regulation mechanism.

Background: Ischemic stroke (IS) is a highly heterogeneous disease with variable pathogenesis. Due to the lack of early predictive markers, the mortality rate of IS remains high worldwide. This study focused on the expression pattern of long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) and its prognostic value in IS. Methods: Twenty-four ICR mice (30-35g, 12 males and 12 females) were involved in this study. Middle cerebral artery occlusion (MCAO) was established to simulate an IS environment. Oxygen-glucose deprivation/reoxygenation (OGD/R) in cells were also performed. A total of 215 IS patients and 153 age and gender-matched controls were included. Quantitative Real-time PCR (qRT-PCR) was performed to detect the expression of MEG3 in peripheral blood leukocytes. Results: The MEG3 expression in MCAO group was significantly higher than control group (P=0.004), and the survival time of high MEG3 group was significantly lower than that of the low MEG3 group (P=0.042). OGD/R promotes cell apoptosis, while si-MEG3 inhibits apoptosis. Results of WB showed that, expression level of Bax was down regulated by si-MEG3, while OGD/R increased its expression level. MEG3 was significantly up-regulated in IS patients and associated with the National Institutes of Health Stroke Scale (NIHSS) (r=0.347, P

TP53-induced glycolysis and apoptosis regulator (TIGAR) activates the pentose phosphate pathway (PPP), which feeds reduced nicotinamide adenine dinucleotide phosphate (NADPH) to the antioxidant glutathione pathway. Oxidative stress-induced neuronal apoptosis is the pathological basis of several neurological disorders, including epilepsy. To determine the potential anti-epileptic action TIGAR in a rodent kainic acid (KA)-induced seizure model. Seizures were induced by the intra-cerebroventricular injection of KA, followed by injection of empty or TIGAR-expressing lentiviral vectors. Immunofluorescence was used to detect the localization of TIGAR in the cortices and hippocampi, and the expression levels of relevant proteins were determined by Western blotting. Oxidative stress-related markers were detected using commercially available kits. Neuronal apoptosis was detected by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) staining. TIGAR were mainly expressed in the neurons and rarely located in the astrocytes, and increased in the cortices and hippocampi of KA-treated rats in a time-dependent manner. Lentivirus-mediated TIGAR overexpression significantly decreased the oxidative stress and neuronal apoptosis induced by KA, resulting in prolonged seizure latency and lower Racine scores. Our findings indicate that TIGAR has anti-epileptic, anti-oxidant and anti-apoptotic effects, and is therefore a promising therapeutictarget for epilepsy.

Background:Bilirubin has been recognized as a potential endogenous inhibitor of atherosclerosis, being inversely associated with carotid intima-media thickness (CIMT). However, little information is available concerning the correlation between serum indirect bilirubin (IBIL), especially long-term IBIL level, and early atherosclerosis progression. This study was designed to evaluate the relationship between serum IBIL level and CIMT progression.Methods:A total of 2205 participants were enrolled in this Asymptomatic Polyvascular Abnormalities Community study (APAC study). CIMT was measured at baseline and 2-year follow-up. The participants were divided into four groups based on their serum IBIL levels at baseline. Both baseline and average serum IBIL values during the 2-year follow up were used in the analysis. Multivariable logistic regression and linear regression were used to assess the associations between serum IBIL and CIMT progression.Results:The results showed that 51.93% (1145/2205) of participants were diagnosed with CIMT progression during the 2-year follow-up. Baseline serum IBIL level was significantly associated with the incidence of CIMT progression after adjusting for other potential confounding factors. Compared with the first quartile, adjusted odds ratios (OR) of the second, third, and fourth quartiles of IBIL were 0.70 [95% confidence interval (CI), 0.55-0.90], 0.68 (95% CI, 0.52-0.87), and 0.63 (95% CI, 0.49-0.82) (P = 0.0006), respectively. Serum IBIL level during the follow-up was also associated with CIMT progression in the univariate analysis (P = 0.0022), although no longer significant after adjusting for potential confounders in the multiple linear regression.Conclusion:The study demonstrated the inverse relationship between serum IBIL and CIMT progression. Lower serum IBIL level is an independent predictor of subclinical atherosclerosis.

Resin tapping could affect water and nutrient transport processes in Chinese pine trees, rendering them more vulnerable to extreme climatic events, such as drought, and affecting the ecological function of forests in semi-arid regions. This study evaluated how resin tapping affects the tree-ring growth and climate sensitivity of Chinese pine in the Loess Plateau. We compared tree-ring growth patterns between the tapped and untapped faces of tapped trees, and investigated tree-ring growth and its response to climate between tapped and untapped trees in a forest stand during the 1967–2017 period. Tapped trees showed asymmetrical growth patterns after resin tapping, with narrower rings near the tapped face and wider ones near the untapped face. Furthermore, tapped trees had inter-annual variations consistent with those of untapped trees except for the years 2000 and 2001, with significantly lower values following resin tapping, and tree-ring growth then returning to normal. The climate response analysis indicated that the tree-ring growth of both tapped and untapped trees was negatively affected by monthly mean temperatures during the early growing season (May to July) in the post-resin-tapping period. Furthermore, tree-ring growth in tapped trees also revealed significant correlation with water vapour deficit and the Palmer drought index, which indicates that tapped trees are more vulnerable to drought. Further studies based on stable isotopes (i.e. δ13C, δ18O, and δ15N) could improve our understanding of the physiological mechanisms that regulate the effects of resin tapping on tree-ring growth.

The underlying mechanisms of arterial remodeling (AR) remain unclear. Studies have indicated that decellularized scaffolds stimulate the differentiation of fibroblasts into myofibroblasts and promote the accumulation of the extracellular matrix (ECM). In the present study, the impact of ECM changes following AR on vascular smooth muscle cell (VSMC) phenotypes was investigated. VSMCs were co-cultured with normal or calcified decellularized arterial scaffolds. The expression levels of α-smooth muscle actin (α-SMA) and osteopontin (OPN) were measured at 2, 5, 10, 15 and 21 days following the establishment of the co-culture systems. The expression of α-SMA in the normal co-culture group was significantly increased compared with that in the calcified arterial decellularized scaffold co-culture group (P

Acclimatization to high-altitude, long-term hypoxia (LTH) reportedly alters cerebral artery contraction-relaxation responses associated with changes in K+ channel activity. We hypothesized that to maintain oxygenation during LTH, basilar arteries (BA) in the ovine adult and near-term fetus would show increased large-conductance Ca2+ activated potassium (BK) channel activity. We measured BK channel activity, expression, and cell surface distribution by use of patch-clamp electrophysiology, flow cytometry, and confocal microscopy, respectively, in myocytes from normoxic control and LTH adult and near-term fetus BA. Electrophysiological data showed that BK channels in LTH myocytes exhibited 1) lowered Ca2+ set points, 2) left-shifted activation voltages, and 3) longer dwell times. BK channels in LTH myocytes also appeared to be more dephosphorylated. These differences collectively make LTH BK channels more sensitive to activation. Studies using flow cytometry showed that the LTH fetus exhibited increased BK β1 subunit surface expression. In addition, in both fetal groups confocal microscopy revealed increased BK channel clustering and colocalization to myocyte lipid rafts. We conclude that increased BK channel activity in LTH BA occurred in association with increased channel affinity for Ca2+ and left-shifted voltage activation. Increased cerebrovascular BK channel activity may be a mechanism by which LTH adult and near-term fetal sheep can acclimatize to long-term high altitude hypoxia. Our findings suggest that increasing BK channel activity in cerebral myocytes may be a therapeutic target to ameliorate the adverse effects of high altitude in adults or of intrauterine hypoxia in the fetus.

An activated carbon nanofiber (ACNF) with high surface area and excellent phenol adsorption capacity has been successfully fabricated by solution blowing of polyacrylonitrile (PAN) into precursor nanofiber which was subsequently activated to ACNF via KOH activation process. The effects of impregnation ratio and activation temperature on the texture properties of ACNF were discussed. The texture properties were characterized by N2 adsorption–desorption isotherm. ACNF showed high value of special surface area and pore volume (2921.263 m2 g−1 and 2.714 cm3 g−1, respectively). The ACNF samples were used for phenol adsorption from aqueous solutions. Adsorption isotherms at 38 °C were fitted with Langmuir and Freundlich models. The relationship between texture properties and phenol adsorption behavior was investigated. As a result, ACNF sample with large surface area, high micropore volume and pore size close and above to 0.43 nm showed the maximum phenol adsorption capacity of 251.6 mg g−1.

ZrO 2 is an important ceramic material, which could be applied into many fields including structural materials, filtration, catalyst support, solar cells and batteries. This paper reported that ZrO 2 fiber mats can be fabricated by solution blowing process and a subsequent calcination process. During the solution blowing process, as-spun PVP/ZrOCl 3 composite fibers were formed after solvent evaporation and stretching of gas flow. These fibers could be subsequently converted into ZrO 2 fibers via calcination process in air at 800 °C. Diameter of these ZrO 2 ceramic fibers could be controlled in the range from 8 to 20 μm by changing parameters, such as the PVP concentration, ZrOCl 3 concentration, gas pressure, the needle size, and the injection rate of the precursor solution.

Objective To analyze the positive predictive value of large artery occlusion and clinical prognosis in acute ischemic stroke patients with total anterior circulation infarct (TACI) who underwent endovascular treatment in the absence of multimodal CT angiography or CT perfusion. Methods The inclusion criteria for the acute ischemic stroke patients to receive endovascular treatment were as the follows: the Oxfordshire Community Stroke Project classification was TACI, Alberta Stroke Program Early Computed Tomography Score (ASPECTS) ≥ 6, National Institutes of Health stroke scale (NIHSS) score ≥8, and less than 4.5 hours since stroke onset. The endovascular treatment was performed on patients who met the inclusion criteria. The endovascular treatment included intra-arterial thrombolysis, mechanical treatments, or both. A retrospective analysis was performed on all eligible acute ischemic stroke patients who underwent endovascular treatment from January 1, 2015 to December 31, 2015. Results A total of 17 patients met the inclusion criteria and underwent endovascular treatment. The median age was 76 years (range, 59–88 years). 12 patients (70.6%) were diagnosed with atrial fibrillation. 16 patients were diagnosed with large artery occlusion by digital subtraction angiography, and the positive predictive value was 94.1%. 16 patients (94.1%) had recanalization (TICI Grade 3); 12 patients (70.6%) had a modified Rankin Scale score of 0–2, and 1 patient (5.9%) died 90 days after treatment. Conclusions In the absence of multimodal CT, endovascular treatment might be beneficial to patients with TACI acute ischemic stroke within 4.5 hours of stroke onset, who had NIHSS score of 8 or greater and ASPECTS of 6 or greater. These inclusion criteria have a high positive predictive value for anterior circulation large artery occlusion.

Solution blowing process is a new nanofiber fabricating method with high productivity. In the present study, nylon 6 nanofiber mats were solution blown and the effects of spinning conditions on nanofibers morphology were investigated. The fiber diameter ranged from 150 to 750 nm which was affected by solution concentration, gas pressure and solution feeding rate. The solution blown fibers were three-dimensional curly which made loose construction in bulk. The filtration performance of solution blown mats was evaluated. The tested solution blown nanofiber mats showed high filtration efficiency of 83.10 % to 93.45 % for 0.3 µm particles filtration and extremely low pressure drop of 15.37 to 30.35 Pa. The results indicate the solution blown nanofiber mats will find potential application of high efficiency and low resistance filter.

Ryanodine receptor (RyR) activity causes Ca2+ sparks in cerebral arterial myocytes by activating adjacent Ca2+-activated K+ (BK) channels, which can dilate arteries. Previous studies show ontogeny increases Ca2+ sparks and long-term hypoxia (LTH) increases BK channel activity. We hypothesized that BK channel activity is greater in arterial myocytes of the LTH fetus than adult due to greater spark activity, and because BK channel clustering is greater in regions where sparks occur. To address this hypothesis we examined spark activity and BK channel clustering to sites of potential spark activity. This was accomplished using line-scan and immunofluorescence techniques, respectively, in basilar arteries from LTH fetal (FH) and adult sheep (AH) kept at 3,801 m for > 100 days. The percentage of myocytes with sparks was ~ 2-fold greater in FH versus AH and unaffected by 30 mM K (30K). Spark amplitude was 7% greater in FH 30K versus AH 30K, while no spatial or temporal changes to sparks were observed. BK channe...