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1.
Neurotox Res ; 2020 Feb 08.
Artigo em Inglês | MEDLINE | ID: mdl-32034697

RESUMO

The effect of plasma endostatin on cognitive impairment after ischemic stroke remains unclear. We conducted this study to explore the association between plasma endostatin in the acute phase of ischemic stroke and post-stroke cognitive impairment (PSCI). Baseline plasma endostatin levels were measured, and cognitive function status was assessed by Montreal cognitive assessment at 3 months among 613 ischemic stroke patients. PSCI was defined as Montreal cognitive assessment score less than 26. The association of endostatin with PSCI was analyzed by logistic regression model. The receiver operating characteristic curve was applied to explore the optimal cutoff value of plasma endostatin levels in predicting PSCI. In a multivariable-adjusted model, the odds ratio for the highest vs lowest quartile of endostatin was 2.01 (95% CI, 1.15-3.53) for PSCI. Restricted cubic spline regression model showed a linear dose-response association between endostatin and PSCI (p for linearity = 0.01). The optimal cut point of endostatin was 84.22 ng/mL; higher endostatin levels (≥ 84.22 ng/mL) were associated with increased risk of 2.17-fold for PSCI (adjusted odds ratio, 2.17; 95% CI, 1.44-3.26; p = 0.0002). Furthermore, adding endostatin to a model containing conventional factors led to significant reclassification for PSCI (net reclassification improvement, 0.20; p = 0.025; integrated discrimination improvement, 0.016; p = 0.002). Our findings showed that elevated plasma endostatin levels were associated with cognitive impairment at 3 months after acute ischemic stroke, independently of established conventional risk factors, suggesting that endostatin may be an important biomarker of cognitive impairment after ischemic stroke.

2.
Brain Res Bull ; 157: 90-99, 2020 Feb 01.
Artigo em Inglês | MEDLINE | ID: mdl-32017970

RESUMO

Diabetic cardiac autonomic neuropathy (DCAN) is a serious complication of diabetes mellitus, which often leads to cardiac dysfunction and even threatens patients' life. Osthole, a natural coumarin derivative, has anti-inflammatory, anti-oxidant and antihypertensive effects. The P2X3 receptor is related to DCAN. The objective of this study will investigate whether osthole relieves DCAN associated with the P2X3 receptor in the stellate ganglia of diabetic rats. A type 2 diabetes mellitus rat model was induced by a combination of diet and streptozotocin. Our results showed that osthole improved the abnormal changes of blood pressure, heart rate, and heart rate variability in diabetic rats and significantly reduced the up-regulated expression levels of the P2X3 receptor, tumor necrosis factor-α and interleukin-1ß in stellate ganglia of diabetic rats. Meanwhile, osthole significantly decreased the elevated serum adrenaline concentration and phosphorylation level of extracellular regulated protein kinase 1/2. In addition, the molecular docking result indicated that osthole was a perfect fit for interacting with the P2X3 receptor. Overall, osthole alleviates the sympathetic relative excitation via inhibiting the expression of P2X3 receptors in the stellate ganglia, to achieve a balance between sympathetic and parasympathetic nerves, relieves the DCAN.

3.
Cancer Res ; 2020 Feb 17.
Artigo em Inglês | MEDLINE | ID: mdl-32066565

RESUMO

Esophageal squamous cell carcinoma (ESCC) is one of the deadliest malignant diseases. Multiple studies with large clinic-based cohorts have revealed that variations of phospholipase C epsilon 1 (PLCE1) correlate with esophageal cancer susceptibility. However, the causative role of PLCE1 in ESCC has remained elusive. Here, we observed that hypomethylation-mediated upregulation of PLCE1 expression was implicated in esophageal carcinogenesis and poor prognosis in ESCC cohorts. PLCE1 inhibited cell autophagy and suppressed the protein expression of p53 and various p53-targeted genes in ESCC. Moreover, PLCE1 decreased the half-life of p53 and promoted p53 ubiquitination, whereas it increased the half-life of mouse double minute 2 homolog (MDM2) and inhibited its ubiquitination, leading to MDM2 stabilization. Mechanistically, the function of PLCE1 correlated with its direct binding to both p53 and MDM2, which promoted MDM2-dependent ubiquitination of p53 and subsequent degradation in vitro. Consequently, knockdown of PLCE1 combined with transfection of a recombinant adenoviral vector encoding wild-type p53 resulted in significantly increased levels of autophagy and apoptosis of esophageal cancer in vivo. Clinically, the upregulation of PLCE1 and mutant p53 protein predicted poor overall survival of ESCC patients, and PLCE1 was positively correlated with p53 in ESCC cohorts. Collectively, this work identified an essential role for PLCE1- and MDM2-mediated ubiquitination and degradation of p53 in inhibiting ESCC autophagy and indicates that targeting the PLCE1-MDM2-p53 axis may provide a novel therapeutic approach for ESCC.

4.
Artigo em Inglês | MEDLINE | ID: mdl-31971766

RESUMO

Environmental pollution, especially air pollution, seriously endangers public health globally. Due to severe air pollution, air filters still face many challenges, especially in terms of filtration performance and filtration stability. Herein, a zeolitic imidazolate framework-8/polypropylene-polycarbonate barklike meltblown fibrous membrane (PPC/ZIF-8) was designed through meltblown and an in situ growth method, achieving efficient PM2.5 capture and high filtration stability under a harsh environment. After in situ growth, the PPC/ZIF-8 membrane could dramatically enhance the PM2.5 filtration efficiency without increasing the pressure drop; the PM2.5 filtration efficiency and quality factor were up to 32.83 and 116.86% higher than those of the pure PPC membrane, respectively. Moreover, through five filtration-wash-dry cycles, the PM2.5 filtration performance is still at a high level. This PPC/ZIF-8 membrane provides a new strategy for the preparation of an air filter with excellent comprehensive filtration performance.

5.
Sci Rep ; 10(1): 990, 2020 Jan 22.
Artigo em Inglês | MEDLINE | ID: mdl-31969619

RESUMO

Microorganisms can utilize biomass to produce valuable chemicals, showing sustainable, renewable and economic advantages compared with traditional chemical synthesis. As a potential five-carbon platform polymer monomer, 5-aminovalerate has been widely used in industrial fields such as clothes and disposable goods. Here we establish an efficient whole-cell catalysis for 5-aminovalerate production with ethanol pretreatment. In this study, the metabolic pathway from L-lysine to 5-aminovalerate was constructed at the cellular level by introducing L-lysine α-oxidase. The newly produced H2O2 and added ethanol both are toxic to the cells, obviously inhibiting their growth. Here, a promising strategy of whole-cell catalysis with ethanol pretreatment is proposed, which greatly improves the yield of 5-aminovalerate. Subsequently, the effects of ethanol pretreatment, substrate concentration, reaction temperature, pH value, metal ion additions and hydrogen peroxide addition on the whole-cell biocatalytic efficiency were investigated. Using 100 g/L of L-lysine hydrochloride as raw material, 50.62 g/L of 5-aminovalerate could be excellently produced via fed-batch bioconversion with the yield of 0.84 mol/mol. The results show that a fast, environmentally friendly and efficient production of 5-aminovalerate was established after introducing the engineered whole-cell biocatalysts. This strategy, combined with ethanol pretreatment, can not only greatly enhance the yield of 5-aminovalerate but also be applied to the biosynthesis of other valuable chemicals.

6.
Biosci Biotechnol Biochem ; : 1-8, 2020 Jan 20.
Artigo em Inglês | MEDLINE | ID: mdl-31959058

RESUMO

Pituitary adenomas constitute one of the most common intracranial tumors. MicroRNAs play an important role in development and progression of pituitary adenomas. In this study, we showed that miR-219a-2-3p was significantly down-regulated in pituitary adenomas cells. Overexpression of miR-219a-2-3p suppressed the proliferation and promoted apoptosis of pituitary adenomas cells. After bioinformatics analysis, we found that MDM2 was one of the downstream targets of miR-219a-2-3p. Further researches showed that miR-219a-2-3p could reduce the protein level of MDM2 by binding to the 3'-UTR of MDM2 and promoted p53 expression. Then, we overexpressed both miR-219a-2-3p and MDM2 in the same group and found that it could counteract the effect of overexpressing miR-219a-2-3p alone on proliferation and apoptosis of pituitary adenoma cells. Taken together, these results suggested that miR-219a-2-3p regulated the proliferation and apoptosis by targeting MDM2/p53 in pituitary adenomas. Therefore, miR-219a-2-3p may serve as a novel marker and therapeutic target for pituitary adenomas.

7.
J Neuroinflammation ; 17(1): 12, 2020 Jan 09.
Artigo em Inglês | MEDLINE | ID: mdl-31918729

RESUMO

BACKGROUND: Dickkopf-3 (Dkk-3) is implicated in the progression of atherosclerosis. This study aimed to investigate the association between serum Dkk-3 and the prognosis of ischemic stroke. METHODS: We measured serum Dkk-3 levels in 3344 ischemic stroke patients from CATIS (China Antihypertensive Trial in Acute Ischemic Stroke). The primary outcome was a combination of death and vascular events within 3 months after ischemic stroke. RESULTS: During 3 months of follow-up, the cumulative incidence rates of primary outcome among ischemic stroke patients in five quintiles of serum Dkk-3 (from low to high) were 4.49%, 3.74%, 2.54%, 5.23%, and 6.73%, respectively (log-rank p = 0.004). Multivariable Cox proportional hazards regression analyses showed that compared with the third quintile of serum Dkk-3, the adjusted hazard ratios (95% confidence intervals) associated with the first and fifth quintile were 3.49 (1.46-8.34) and 4.23 (1.86-9.64) for primary outcome, 3.47 (1.06-11.36) and 5.30 (1.81-15.51) for death, and 2.66 (1.01-7.01) and 3.35 (1.33-8.40) for vascular events, respectively. Multivariable-adjusted Cox proportional hazards regression model with restricted cubic splines showed a U-shaped association between serum Dkk-3 and the risk of primary outcome (p for nonlinearity = 0.030). Moreover, adding serum Dkk-3 to conventional risk factors could improve the predictive power for primary outcome (net reclassification improvement 28.44%, p < 0.001; integrated discrimination improvement 0.48%, p = 0.001). CONCLUSIONS: Both low and high serum Dkk-3 levels are associated with increased risks of death and vascular events within 3 months after ischemic stroke, indicating that serum Dkk-3 may have a special effect on the prognosis of ischemic stroke. We also found that serum Dkk-3 might be a prognostic biomarker for ischemic stroke. Further studies are needed to replicate our findings and to determine the optimal levels of serum Dkk-3.

8.
Bioresour Technol ; 297: 122413, 2020 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-31761628

RESUMO

MgO/N-doped active carbon (Mg/N-C) derived from sugarcane bagasse was prepared for the removal of methyl orange (MO). Mg/N-C composites presented the better adsorption capacity than that of active carbon and N-doped active carbon, of which the maximum adsorption capacity of 2-Mg/N-C-b2 for the MO removal is 384.61 mg g-1. The effects of MgO dosage, N-doped content, pyrolysis temperature, pH value, inorganic ions and solution temperature on the adsorption performance of Mg/N-C composites in the MO removal were investigated in detail. The pseudo-second order model and Langmuir isotherm model fitted well with the adsorption kinetics and isotherms of Mg/N-C. The rate-determining step was the boundary diffusion and intra-particle diffusion. The adsorption process of 2-Mg/N-C-b2 was a spontaneous and physisorption process.


Assuntos
Saccharum , Poluentes Químicos da Água , Adsorção , Carbono , Celulose , Concentração de Íons de Hidrogênio , Cinética , Óxido de Magnésio
9.
Med Phys ; 47(1): 190-200, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31661161

RESUMO

PURPOSE: While cone beam computed tomography (CBCT) is able to provide patient anatomical information, its image quality is severely degraded due to scatter contamination, which degrades the accuracy of CBCT-based dose distribution estimation in proton therapy. In this work, we combined two existing scatter kernel correction methods: the point-spread function (PSF)-based scatter kernel derivation method and the fast adaptive scatter kernel superposition (fASKS) model, and evaluated the impact of the modified fASKS (mfASKS) correction on the accuracy of proton dose distribution estimation. To evaluate feasibility of the mfASKS approach using accurate scatter distributions, both Monte Carlo simulations and experiments were performed for an on-board CBCT machine integrated with a proton therapy machine. METHODS: We developed a strategy to modify central intensity, constant intensity, and amplitude of the scatter kernels derived from PSFs for the fASKS model. A parameter required for the fASKS model was derived by optimizing uniformity in the mfASKS-corrected reconstructed images. Subsequently, the mfASKS model was used to remove scatter in CBCT imaging. We quantitatively compared the Hounsfield Unit (HU) and proton stopping power ratio (SPR) images for five different phantoms. To assess improvement of dose calculation accuracy, a series of proton treatment plans were produced using the CBCT images with and without the mfASKS correction. RESULTS: The accuracies of both HU and SPR intensity quantifications are improved as a result of the mfASKS correction. Mean absolute water-equivalent path length difference to the true value decreases from 10.3 to 0.934 mm for the Gammex phantom (simulation). At the same time, mfASKS is able to offer more accurate dose distributions, especially at the distal fall-off region where noticeable dose overestimation is observed in the uncorrected scenario. Mean absolute relative error of proton range in the pelvic phantom improves from 5.03% to 2.57% (experiment). CONCLUSIONS: mfASKS enables more accurate CBCT-based proton dose calculation. This technique has significant implications in image-guided radiotherapy and dose verifications in adaptive proton therapy.

10.
J Cell Physiol ; 235(4): 3886-3893, 2020 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-31603257

RESUMO

Non-small-cell lung cancer (NSCLC) is the most common malignancy along with high mortality rate worldwide. Recently, nucleolar and spindle-associated protein 1 (NUSAP1) has been reported to be involved in the malignant progression of several cancers. However, in NSCLC, the biological function of NUSAP1 and its molecular mechanism have not been reported. Here, our findings indicated that the NUSAP1 messenger RNA expression level was remarkably upregulated in NSCLC tissues compared with that of adjacent normal tissues. We also found that NUSAP1 gene expression was notably upregulated in NSCLC cell lines (A549, 95-D, H358, and H1299) compared with that of normal human bronchial epithelial cell line (16HBE). Subsequently, the biological function of NUSAP1 was investigated in A549 and H358 cells transfected with NUSAP1 small interfering RNA (siRNA), respectively. Results showed that NUSAP1 knockdown inhibited NSCLC cell proliferation, and promoted cell apoptosis. Furthermore, the number of cell migration and invasion was significantly suppressed by NUSAP1 knockdown. In addition, our results indicated that NUSAP1 knockdown increased the gene expression of B-cell translocation gene 2 (BTG2), but decreased the expression levels of phosphoinositide 3-kinase (PI3K) and phosphorylated serine/threonine kinase (p-AKT). BTG2 siRNA partly abrogates the effect of NUSAP1 knockdown on BTG2 gene expression. Fumonisin B1 (FB1), a AKT activator, reversed the effect of NUSAP1 knockdown on the biological function in NSCLC. Taken together, NUSAP1 knockdown promotes NSCLC cell apoptosis, and inhibits cell proliferation, cell migration, and invasion, which is associated with regulating BTG2/PI3K/Akt signal pathway. Our findings suggest that NUSAP1 is a promising molecular target for NSCLC treatment.

11.
J Exp Bot ; 71(3): 970-985, 2020 Jan 23.
Artigo em Inglês | MEDLINE | ID: mdl-31639820

RESUMO

Brassinosteroids (BRs) are a group of steroid hormones regulating plant growth and development. Since BRs do not undergo transport among plant tissues, their metabolism is tightly regulated by transcription factors (TFs) and feedback loops. BAS1 (CYP734A1, formerly CYP72B1) and SOB7 (CYP72C1) are two BR-inactivating cytochrome P450s identified in Arabidopsis thaliana. We previously found that a TF ATAF2 (ANAC081) suppresses BAS1 and SOB7 expression by binding to the Evening Element (EE) and CIRCADIAN CLOCK ASSOCIATED 1 (CCA1)-binding site (CBS) on their promoters. Both the EE and CBS are known binding targets of the circadian regulatory protein CCA1. Here, we confirm that CCA1 binds the EE and CBS motifs on BAS1 and SOB7 promoters, respectively. Elevated accumulations of BAS1 and SOB7 transcripts in the CCA1 null mutant cca1-1 indicate that CCA1 is a repressor of their expression. When compared with either cca1-1 or the ATAF2 null mutant ataf2-2, the cca1-1 ataf2-2 double mutant shows higher SOB7 transcript accumulations and a stronger BR-insensitive phenotype of hypocotyl elongation in white light. CCA1 interacts with ATAF2 at both DNA-protein and protein-protein levels. ATAF2, BAS1, and SOB7 are all circadian regulated with distinct expression patterns. These results demonstrate that CCA1 and ATAF2 differentially suppress BAS1- and SOB7-mediated BR inactivation.

12.
Atherosclerosis ; 293: 42-48, 2020 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-31835040

RESUMO

BACKGROUND AND AIMS: Endostatin is implicated in the atherosclerosis process and serves as a promising cardiovascular biomarker, while its clinical significance in ischemic stroke patients remains unclear. We aimed to examine the association between endostatin and mortality and disability after ischemic stroke. METHODS: A total of 3463 acute ischemic stroke patients with measured plasma endostatin from the China Antihypertensive Trial in Acute Ischemic Stroke were included in this study. The primary outcome was death or severe disability (modified Rankin scale score of 4-6), and secondary outcomes included death and vascular events. RESULTS: After 3-month follow-up, 402 (11.61%) participants experienced severe disability or died. Compared with the lowest quartile of endostatin, odds ratios or hazard ratios (95% confidence intervals) for the highest quartile were 1.47 (1.04-2.09) for the primary outcome, and 2.36 (1.23-4.54) for death after adjustment for multiple covariates, including age, sex, admission NIH Stroke Scale score and systolic blood pressure. Each 1-SD higher log-transformed endostatin was associated with a 20% (6%-36%) increased risk for primary outcome. Adding plasma endostatin to the basic model constructed with conventional factors significantly improved risk stratification of primary outcome, as observed by the category-free net reclassification index of 20.5% (95% CI 10.1%-30.8%; p < 0.001) and integrated discrimination improvement of 0.3% (95% CI 0.01%-0.6%; p = 0.04). CONCLUSIONS: Increased baseline plasma endostatin levels in acute ischemic stroke were associated with increased risk of mortality and severe disability at 3 months. Plasma endostatin may serve as an important prognostic marker for risk stratification in patients with ischemic stroke.

13.
Oncol Lett ; 18(6): 5968-5976, 2019 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-31788071

RESUMO

Lung cancer is the most common cause of cancer-associated mortality globally. Long non-coding RNAs (lncRNAs) are transcripts with a length of >200 nucleotides, which are not translated into proteins. Growing evidence has indicated that certain lncRNAs are associated with various biological processes in cancer. However, the functions of KCNK15 and WISP2 antisense RNA 1 (KCNK15-AS1) in lung cancer carcinogenesis and progression have remained elusive. The present study indicated that KCNK15-AS1 was overexpressed in lung adenocarcinoma tissues compared with paracancerous normal tissues, and the high expression of KCNK15-AS1 was significantly associated with poor prognosis compared with the patients with low expression (P<0.001). Furthermore, the knockdown of KCNK15-AS1 was performed in A549 and H460 lung cancer cells with small interfering RNA, resulting in a significant inhibition of the proliferation, a decrease in the mRNA and protein expression of cyclin D1 (CCND1) and epidermal growth factor receptor (EGFR), in addition to the phosphorylation of protein kinase B, with a concomitant increase in the expression of microRNA (miR)-202 and miR-370 compared with negative control group. Rescue experiments demonstrated that the inhibition of miR-202 or miR-370 partially recovered the EGFR and CCND1 expression and the proliferation rates, which were reduced by KCNK15-AS1 silencing. In conclusion, these results suggested that KCNK15-AS1 functions as an oncogene via regulating the miR-202/miR-370/EGFR axis in lung cancer and may provide a potential target for lung cancer treatment.

14.
Artigo em Inglês | MEDLINE | ID: mdl-31794839

RESUMO

PURPOSE: To compare long-term survival outcomes and sequelae between children and adult nasopharyngeal carcinoma (NPC) in the era of intensity-modulated radiotherapy (IMRT). METHODS AND MATERIALS: Data on 285 NPC patients aged ≤ 18 years old at diagnosis and treated with IMRT between January 2004 and November 2016 were retrospectively reviewed. Propensity score matching method was adopted to screen matched adult NPC patients at a ratio of 1:3. Survival outcomes and treatment-related toxicities between children and adult groups were compared. RESULTS: In total, 159 children and 477 adult NPC patients were included in this study. The 5-year overall survival (OS), distant metastasis-free survival (DMFS), locoregional relapse-free survival (LRRFS), and disease-free survival (DFS) between children and adult were 89.2% vs 83.6% (P = 0.144), 88.7% vs 83.5% (P = 0.124), 96.4% vs 89.1% (P = 0.013), and 86.5% vs 77.3% (P = 0.021), respectively. Subgroup analyses revealed that the young age was an independent prognostic factor of OS, DMFS and LRRFS in advanced N stage (N2-3) group, and DFS in advanced T stage (T3-4) group, N2-3 and stage III-IVA groups. The most common sequela was ototoxicity (68.9%) in children patients and xerostomia (70.8%) in adult patients. Adult survivors had a significantly higher incidence of grade 3-4 late toxicities in xerostomia (17.6% vs. 8.9%, P = 0.004), skin dystrophy (9.3% vs. 3.7%, P = 0.022), neck fibrosis (8.3% vs. 4.4%, P < 0.001) and radiation encephalopathy (0.8% vs. 0, P = 0.006). Children survivors were more likely to develop grade 3-4 growth retardation and endocrine insufficiency (3.0% vs. 0.3%, P = 0.014). CONCLUSIONS: Children NPC patients achieved significantly better survival outcomes but less late toxicities than adult patients. However, we should pay great attention to growth problems of children survivors.

15.
Clin Interv Aging ; 14: 1937-1946, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31806949

RESUMO

Aim: Fasting glucose has been associated with vascular aging, but the association between HbA1c and vascular aging has been limitedly studied in Chinese and other ethnic populations. We aimed to examine this association in a large sample of Chinese adults. Methods: In the Tianning Cohort (N=5142), fasting glucose, HbA1c, carotid-femoral pulse wave velocity (cfPWV), and pulse pressure (PP) were measured. Vascular aging was defined as having the highest quartile level of cfPWV or PP. We applied quantile regression models to examine the association between glucose metabolism and vascular aging. Results: The median cfPWV was significantly increased as increasing quintiles of fasting glucose (ß=0.14, P<0.001) and HbA1c (ß=0.07, P=0.0056), respectively. Per 1-mmol/L increment of fasting glucose was significantly associated with a higher risk of having vascular aging defined by cfPWV (OR=1.05, P=0.022), PP (OR=1.06, P=0.048), or either (OR=1.08, P=0.002). Similarly, per 1% increment of HbA1c was significantly associated with a higher risk of having vascular aging defined by cfPWV (OR=1.06, P=0.044), PP (OR=1.10, P=0.012), or either (OR=1.12, P=0.042). Conclusion: Glucose metabolism was significantly and positively associated with vascular aging in Chinese adults, but the causality is uncertain.

16.
Artigo em Inglês | MEDLINE | ID: mdl-31831364

RESUMO

BACKGROUND AND AIMS: High serum hepatocyte growth factor (HGF) levels increase the risk of ischemic stroke and are probably associated with outcomes after ischemic stroke. However, it remains unclear whether the association between HGF and ischemic stroke prognosis is modified by blood lipid status. METHODS AND RESULTS: Data were derived from the CATIS (China Antihypertensive Trial in Acute Ischemic Stroke), and we measured baseline serum HGF levels in 3027 ischemic stroke patients. The primary outcome was a combination of death and major disability (modified Rankin Scale score≥3) at 2 years after ischemic stroke. Blood lipid status could modify association between HGF and ischemic stroke prognosis (Pinteraction = 0.002). After multivariate adjustment, the odds ratios of primary outcome associated with the highest tertile of HGF were 2.13 (95% CI, 1.45-3.14; Ptrend<0.001) for patients with dyslipidemia and 0.81 (95% CI, 0.54-1.22; Ptrend = 0.310) for those with normal lipids. Adding HGF to conventional risk factors improved risk prediction for primary outcome in patients with dyslipidemia (net reclassification improvement: 24.28%, P < 0.001; integrated discrimination index: 0.43%, P = 0.022) but not in those with normal lipids. Secondary analyses further revealed that HDL-C was the main lipid component to modify the prognostic significance of serum HGF among ischemic stroke patients. CONCLUSIONS: There was a modified effect of blood lipid status on the association between serum HGF and ischemic stroke prognosis. Elevated serum HGF was associated with outcomes in ischemic stroke patients with dyslipidemia, especially low HDL-C. Further studies are warranted to replicate our findings and clarify the potential biological mechanisms.

17.
J Hypertens ; 2019 Dec 12.
Artigo em Inglês | MEDLINE | ID: mdl-31834126

RESUMO

OBJECTIVES: Although hyperuricemia, microalbuminuria, and hypertension are highly correlated, their temporal relationship is largely unknown. We aimed to examine whether microalbuminuria mediated the association between hyperuricemia and hypertension. METHODS: Leveraging a longitudinal cohort including 1981 Chinese adults who had blood pressures, urinary albumin to creatinine ratio (UACR), and uric acid measured twice 4 years apart, we examined the temporal relationships among hyperuricemia, microalbuminuria, and hypertension by cross-lagged panel analysis followed by a causal mediation analysis to confirm the temporal consequence. Age, sex, education level, cigarette smoking, alcohol consumption, obesity, blood glucose, and lipids were adjusted. RESULTS: The cross-lagged panel analysis demonstrated that the relationship from baseline UACR to follow-up uric acid was significantly smaller than that from baseline uric acid to follow-up UACR (ß: 0.010 vs. 0.054, P < 0.001). The relationships from baseline blood pressures to follow-up UACR were also significantly smaller than that from baseline UACR to follow-up blood pressures (ß: 0.031 vs. 0.092, P < 0.001 for systolic and ß: 0.015 vs. 0.096, P < 0.001 for diastolic). The causal mediation analysis found that UACR partially mediated the association of baseline uric acid with follow-up SBP (mediate proportion: 9.14%, 95% CI: 1.58-23.00%) and DBP (mediate proportion: 7.38%, 95% CI: 1.05-19.00%). CONCLUSION: Microalbuminuria may follow elevated uric acid and partially mediate its effect on future risk of hypertension in Chinese adults.

19.
Front Oncol ; 9: 1208, 2019.
Artigo em Inglês | MEDLINE | ID: mdl-31781503

RESUMO

The treatment of glioblastoma has been a big challenge for decades in the oncological field mainly owing to its unique biological characteristics, such as high heterogeneity, diffusing invasiveness, and capacity to resist conventional therapies. The mRNA-based therapeutic modality holds many superior features, including easy manipulation, rapid and transient expression, and adaptive convertibility without mutagenesis, which are suitable for dealing with glioblastoma's complexity and variability. Synthetic anticancer mRNAs carried by various vehicles act as the ultimate attackers of the tumor across biological barriers. In this modality, specifically targeted glioblastoma treatment can be guaranteed by adding targeting molecules at certain levels. The choice of mRNA-bearing vehicle and administration method is a fully patient-tailored selection. This review covers the advantages and possible limitations of mRNA-based gene therapy, the in vitro synthesis of mRNA, the feasible methods for synthetic mRNA delivery and clinical therapeutic prospects of mRNA-based gene therapy for glioblastoma.

20.
Nanomaterials (Basel) ; 9(12)2019 Nov 21.
Artigo em Inglês | MEDLINE | ID: mdl-31766440

RESUMO

In this work, N-doped carbon-coated ZnS with a sulfur-vacancy defect (ZnS@N-C) was performed for the visible-light-driven photodegradation of tetracycline hydrochloride (TCH). The obtained ZnS@N-C exhibited enhanced photocatalytic activity compared with ZnS for TCH removal. Among these ZnS@N-C composites, ZnS@N-C-3 with N-doped content of 3.01% (100 nm) presented the best visible-light photocatalytic activity and superior long-term photocatalytic stability after five cycle times for TCH removal in the visible light region. This may be ascribed to the interface between the N-doped carbon shell and ZnS with a sulfur-vacancy defect for efficient charge transfer and the restrained recombination of charge carriers. Electron spin resonance (ESR) results indicate that the ·O2‒ radical plays a crucial role in the enhanced photocatalytic activity of ZnS@N-C-3.

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