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1.
Sci Rep ; 9(1): 17641, 2019 Nov 27.
Artigo em Inglês | MEDLINE | ID: mdl-31776411

RESUMO

Kawasaki disease (KD) is a systemic febrile, inflammatory vascular disease of unknown etiology. The coronary artery abnormality (CAA) caused by KD has become the most commonly acquired heart disease in children. Initial treatment of intravenous immunoglobulin (IVIG) can reduce the incidence of CAA. Thrombocytosis is common during the course of KD, but changes in and significances of platelet function and parameters are unclear. In this study, we enrolled 120 patients, including 40 patients with KD, 40 febrile controls, and 40 afebrile controls. The platelet function was assessed using the platelet function analyzer (PFA)-200. Platelet parameters, including platelet count (PLT), mean platelet volume (MPV), platelet distribution width (PDW), and platelet hematocrit (PCT) were measured. In the febrile period, the PDW and MPV were lower in KD patients (P < 0.05). The platelet function did not change significantly during the febrile period of KD but weakened in the defervescence phase. No significant differences between the CAA and normal groups, and between IVIG resistance and response groups. The diagnostic cutoff value of the PDW level for predicting KD was 10.85 fL with a sensitivity of 55% and a specificity of 77.5% (area under curve (AUC) = 0.690, 95% confidence interval (CI): 0.574-0.806, P < 0.01). Besides, the MPV level was 9.55 fL with sensitivity of 75% and specificity of 70% (AUC = 0.733, 95%CI: 0.620-0.846, P < 0.001). This is the first longitudinal study of platelet function changes in KD patients using PFA-200. Besides, lower PDW and MPV may be available markers for early diagnosis of KD.

2.
J Colloid Interface Sci ; 560: 198-207, 2019 Oct 19.
Artigo em Inglês | MEDLINE | ID: mdl-31670017

RESUMO

Solid wastes, such as polystyrene foam waste and silica gel waste which are ubiquitous products have caused serious environmental issues, such as "white pollution", threatening the health of humans and animals. As such, the need to recycle and re-use of solid wastes has attracted increasing attention in the last few years. In this work, a self-healing superhydrophobic coating is successfully fabricated by blending polystyrene foam waste with fluorinated silica gel waste (F-silica gel waste), octadecyltrimethoxysilane (OTMS) modified silica particles (OTMS-silica particles), and near-infrared (NIR) light responsive microcapsules. The F-silica gel waste and OTMS-silica nanoparticles act as hydrophobic fillers meanwhile the polystyrene foam waste acts as a coating binder. The NIR-responsive microcapsules are obtained by the electrostatic adsorption of carbon nanoparticles onto the surface of microcapsules loaded with 1H, 1H, 2H, 2H-perfluorooctyltriethoxysilane. The superhydrophobic property of the coating can be healed after 10 min of NIR irradiation. Additionally, the as-prepared coating can be coated on several different substrates, similar to commercial coatings, and it is seen that its excellent superhydrophobic property is durable and is maintained even when the coating is subjected to a sand-drop test. The self-healing mechanism of the superhydrophobic coatings is also investigated.

3.
Lipids Health Dis ; 18(1): 201, 2019 Nov 18.
Artigo em Inglês | MEDLINE | ID: mdl-31739782

RESUMO

BACKGROUND: Long noncoding RNAs (lncRNAs) are involved in numerous physiological functions. However, their mechanisms in acute myocardial infarction (AMI) are not well understood. METHODS: We performed an RNA-seq analysis to explore the molecular mechanism of AMI by constructing a lncRNA-miRNA-mRNA axis based on the ceRNA hypothesis. The target microRNA data were used to design a global AMI triple network. Thereafter, a functional enrichment analysis and clustering topological analyses were conducted by using the triple network. The expression of lncRNA SNHG8, SOCS3 and ICAM1 was measured by qRT-PCR. The prognostic values of lncRNA SNHG8, SOCS3 and ICAM1 were evaluated using a receiver operating characteristic (ROC) curve. RESULTS: An AMI lncRNA-miRNA-mRNA network was constructed that included two mRNAs, one miRNA and one lncRNA. After RT-PCR validation of lncRNA SNHG8, SOCS3 and ICAM1 between the AMI and normal samples, only lncRNA SNHG8 had significant diagnostic value for further analysis. The ROC curve showed that SNHG8 presented an AUC of 0.850, while the AUC of SOCS3 was 0.633 and that of ICAM1 was 0.594. After a pairwise comparison, we found that SNHG8 was statistically significant (P SNHG8-ICAM1 = 0.002; P SNHG8-SOCS3 = 0.031). The results of a functional enrichment analysis of the interacting genes and microRNAs showed that the shared lncRNA SNHG8 may be a new factor in AMI. CONCLUSIONS: Our investigation of the lncRNA-miRNA-mRNA regulatory networks in AMI revealed a novel lncRNA, lncRNA SNHG8, as a risk factor for AMI and expanded our understanding of the mechanisms involved in the pathogenesis of AMI.

4.
Chemosphere ; 242: 125168, 2019 Oct 24.
Artigo em Inglês | MEDLINE | ID: mdl-31678850

RESUMO

Plants have evolved effective strategies to cope with heavy metals Cd toxicity, but the regulatory mechanism underlying Cd tolerance and accumulation are still poorly understood. miR156 has been shown to be the master regulator of development and stress response in plants. However, whether miR156 is also involved in plant Cd stress response remains unknown. Here, we show that plants overexpressing miR156 (miR156OE) accumulated significantly less Cd in the shoot, and conferred enhanced tolerance to Cd stress. Plants with a knocked-down level of miR156 (MIM156) were sensitive to Cd stress, and accumulated significantly higher Cd. Under Cd stress, miR156OE had significantly longer primary root length, higher biomass and chlorophyll content, increased activities of antioxidative enzymes and lower levels of endogenous reactive oxygen species (ROS), while MIM156 had the opposite phenotype. To investigate the underlying mechanism of miR156-mediated Cd stress response in Arabidopsis, we profiled the expression of several Cd transporter genes. The expression of Cd uptake transporter of AtZIP1、AtZIP2 and vacuole segregated transporter AtABCC1 was significantly elevated in miR156OE, whereas it was significantly reduced in MIM156. MIM156 also led to an elevated level of AtHMA4 responsible for transporting Cd from the root to the shoot. Our results indicate that miR156 acts as a positive regulator of plant tolerance to Cd stress by modulating ROS levels and Cd uptake/transport genes expression. Therefore, our study adds a new layer of regulatory mechanism for Cd transport and tolerance in plants, and provides a perspective to regulate Cd transport artificially by modulating plant vegetative growth and development using miR156.

5.
Cell Death Dis ; 10(11): 833, 2019 Nov 04.
Artigo em Inglês | MEDLINE | ID: mdl-31685801

RESUMO

RBBP6 has been implicated in tumorigenesis but its role in tumor metastasis and progression has not been evaluated. Interestingly, here we show that RBBP6 is upregulated in colorectal cancer (CRC) where its expression level is positively correlated with distant metastasis. In this study, we identified RBBP6, a RING Finger-domain E3 ubiquitin ligase, served as an independent prognostic factor and predicted poor outcome for CRC patients. RBBP6 promoted cell proliferation, migration, and invasion in CRC cells and promoted tumor growth, lung metastasis, and liver metastasis in mouse models. Mechanistically, we revealed that RBBP6 bound and ubiquitylated IκBα, an inhibitor of the NF-κB-signaling pathway. RBBP6-mediated ubiquitination and degradation of IκBα significantly enhanced p65 nuclear translocation, which triggered the activation of NF-κB pathway and then induced the epithelial-mesenchymal transition (EMT) process and cell metastasis. Furthermore, by DNA methylation results and ChIP analysis, we demonstrated that the promoter of RBBP6 was hypomethylated, and was activated by multi-oncogenic transcription factors. In conclusion, our findings suggest that RBBP6 may be a potential prognostic biomarker and therapeutic target for CRC invasion and metastasis.

6.
J Exp Med ; 2019 Nov 07.
Artigo em Inglês | MEDLINE | ID: mdl-31699822

RESUMO

Blood-brain barrier (BBB) dysfunction has been suggested to play an important role in epilepsy. However, the mechanism mediating the transition from cerebrovascular damage to epilepsy remains unknown. Here, we report that endothelial cyclin-dependent kinase 5 (CDK5) is a central regulator of neuronal excitability. Endothelial-specific Cdk5 knockout led to spontaneous seizures in mice. Knockout mice showed increased endothelial chemokine (C-X-C motif) ligand 1 (Cxcl1) expression, decreased astrocytic glutamate reuptake through the glutamate transporter 1 (GLT1), and increased glutamate synaptic function. Ceftriaxone restored astrocytic GLT1 function and inhibited seizures in endothelial Cdk5-deficient mice, and these effects were also reversed after silencing Cxcl1 in endothelial cells and its receptor chemokine (C-X-C motif) receptor 2 (Cxcr2) in astrocytes, respectively, in the CA1 by AAV transfection. These results reveal a previously unknown link between cerebrovascular factors and epileptogenesis and provide a rationale for targeting endothelial signaling as a potential treatment for epilepsy.

7.
Curr Pharm Des ; 2019 Nov 18.
Artigo em Inglês | MEDLINE | ID: mdl-31742493

RESUMO

Chronic kidney disease (CKD) is characterized by gradually loss of renal mass and functions. It has become a global health problem with hundreds of millions people affected. Both its incidence and prevalence are increasing over time. More than $20,000 are spent on each patients per year. The economic burden on the patients as well as the society is heavy. And their life quality becomes worsen over time. However, there are still limited effective therapeutic strategies on CKD. Patients mainly rely on dialysis and renal transplantation, which cannot prevent all the complications of CKD. Great efforts are needed in the understanding the nature of CKD progression as well as developing effective therapeutic methods, including pharmacological agents. This paper reviews three aspects in the research of CKD that may show great interests to those who devote in bioanalysis, biomedicine and drug development, including important endogenous biomarkers quantification, mechanisms underlying CKD progression and current status of CKD therapy.

8.
Int Immunopharmacol ; : 105926, 2019 Nov 05.
Artigo em Inglês | MEDLINE | ID: mdl-31704291

RESUMO

Previous studies indicate that myocardial infarction (MI) may contribute to atrial fibrillation (AF). Emerging evidence has shown that pinocembrin protects myocardial ischemic injury (I/R)-induced cardiac fibrosis and arrhythmias in animals via its anti-inflammatory or antioxidant activities. However, the effects of pinocembrin on MI-induced atrial arrhythmias remain unknown. Thus, this study aimed to investigate the effects of pinocembrin on autonomic dysfunction and AF susceptibility in MI rats and the possible mechanism. In a standard experimental MI model, Sprague-Dawley rats received permanent ligation of the left anterior descending (LAD) coronary artery and were treated with pinocembrin or saline for 6 days. Our results demonstrated that pinocembrin treatment significantly decreased sympathetic activity, augmented parasympathetic activity, improved heart rate variability (HRV), prolonged the atrial effective refractory period (ERP) and action potential duration (APD), shortened activation latency (AL), lowered the indicibility rate of AF, attenuated atrial fibrosis, and decreased concentrations of norepinephrine (NE), tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß and IL-6 in the serum and the left atrial (LA). Furthermore, pinocembrin treatment significantly increased the expression levels of Cx43 and Cav1.2 and suppressed the phosphorylation of inhibitor-κBα (IκBα) and the activation of nuclear factor-kappa B (NF-κB)subunit p65. In conclusion, the findings indicate that pinocembrin treatment decreases autonomic remodeling, lowers atrial fibrosis, ameliorates atrial electrical remodeling, and suppresses MI-induced inflammatory responses, which suggests a potential novel strategy for atrial arrhythmias.

9.
Nat Neurosci ; 2019 Nov 25.
Artigo em Inglês | MEDLINE | ID: mdl-31768050

RESUMO

To discover novel genes underlying amyotrophic lateral sclerosis (ALS), we aggregated exomes from 3,864 cases and 7,839 ancestry-matched controls. We observed a significant excess of rare protein-truncating variants among ALS cases, and these variants were concentrated in constrained genes. Through gene level analyses, we replicated known ALS genes including SOD1, NEK1 and FUS. We also observed multiple distinct protein-truncating variants in a highly constrained gene, DNAJC7. The signal in DNAJC7 exceeded genome-wide significance, and immunoblotting assays showed depletion of DNAJC7 protein in fibroblasts in a patient with ALS carrying the p.Arg156Ter variant. DNAJC7 encodes a member of the heat-shock protein family, HSP40, which, along with HSP70 proteins, facilitates protein homeostasis, including folding of newly synthesized polypeptides and clearance of degraded proteins. When these processes are not regulated, misfolding and accumulation of aberrant proteins can occur and lead to protein aggregation, which is a pathological hallmark of neurodegeneration. Our results highlight DNAJC7 as a novel gene for ALS.

10.
J Toxicol Environ Health A ; : 1-7, 2019 Nov 24.
Artigo em Inglês | MEDLINE | ID: mdl-31760910

RESUMO

Cerium oxide (CeO2), one of many engineered nanomaterials (ENMs), is composed primarily of metal oxides, such as cerium oxide (CeO2). CeO2-containing materials are widely used as a polishing agent for glass mirrors, plate glass, television tubes, ophthalmic lenses, and precision optics. The widespread use of this nanomaterial (NM) resulted in increased environmental contamination levels and consequent human exposure. However, the influence of Ce on humans remains to be determined. The aim of this study was to expose female ICR mice to varying nanoparticle sizes of 35 nm, 300 nm as well as a mixture of 1-5 µM CeO2 particles through intranasal (i.n.) instillation at 40 mg/kg dose on day 1, 3 and 5, and the experiment terminated on day 7. Histopathology findings demonstrated that hydropic degeneration was prominently associated with hemorrhage in renal cortex and medulla in all CeO2-administered groups. In liver of CeO2-exposed mice, hydropic degeneration was also prominent. Serum chemistries also indicated signs of renal and hepatic lesion as evidenced by significantly decreased serum levels of total bilirubin (TBIL) and total phosphate (TP) and activity of alkaline phosphatase (ALP). ICP-MS analysis group demonstrated that Ce levels were not significantly higher in liver and kidneys of mice exposed to 35 nm CeO2. An increase in Ce content was observed in hepatic and renal tissues of mice exposed to 300 nm or 1-5 µM CeO2. The levels of Ce were similar in these two groups suggesting a threshold level of Ce was attained regardless of NP size. Data thus demonstrated that i.n. instillation of different-sized CeO2 particles translocated to liver and kidney and that size difference of CeO2 particles did not exert significant in the observed histopathology responses.

11.
BMC Pulm Med ; 19(1): 199, 2019 Nov 05.
Artigo em Inglês | MEDLINE | ID: mdl-31690305

RESUMO

BACKGROUND: Few studies have reported the placement of metallic Y-shaped covered stents (Y stents) for bronchopleural fistula around the upper carina. METHODS: Eighteen patients were treated with Y stents insertion under the guidance of fluoroscopy. All covered stents were custom-designed and inserted to fit the upper carina anatomy. Clinical data and medical imaging data were analyzed retrospectively. RESULTS: The stents were implanted successfully for the first time in 17 patients, and one patient needed a second attempt due to stent migration during withdrawal of the guide wires. In total, 19 small Y single-plugged stents were inserted in the upper carina and 5 large Y stents additionally in the main carina. Nineteen complications were observed in 14 patients, including 4 major complications. Stents were successfully removed in 12 patients due to complications or cure efficacy, for a median duration in place of 89.5 days. One patient lost follow-up. Nine patients were cured, and three had clinical improvement. One patient died of ventricular fibrillation the second day after the procedure and 4 patients died of tumors 7.8 to 91.7 months after stent placement. The 1-, 3-, and 5-year survival rates were 87.5, 80.8 and 80.8%, respectively. CONCLUSIONS: Metallic Y stent placement is technically feasible, effective and safe for bronchopleural fistula disease around the upper carina.

12.
J Stroke Cerebrovasc Dis ; : 104483, 2019 Nov 11.
Artigo em Inglês | MEDLINE | ID: mdl-31727597

RESUMO

OBJECTIVE: Gastrodin, a glucoside of gastrodigenin, inhibits cerebral oxidant stress and apoptosis in multiple central nervous system injury, but its effect in intracerebral hemorrhage (ICH) remains unclear. This study investigated the effect of gastrodin on neuronal apoptosis and neurological deficits in rat ICH model. METHODS: In vitro experiments were performed using hematoma lysate-induced cell damage model in primary cortical neurons. Rat ICH model was produced by a caudatum injection of collagenase. Gastrodin was intraperitoneal injected after 2 hours following ICH. Cell viability, brain water content, neurological score, western blot, and immunofluorescence experiments were performed. RESULTS: Gastrodin significantly decreased hematoma lysate-induced reduction of cell viability and cell apoptosis in primary cortical neurons. Gastrodin significantly improved brain edema and neurological deficits post-ICH. Moreover, gastrodin administration significantly reduced levels of ROS, 8-OHDG, 3-Nitrotyrosine and MDA, while increased GSH-Px and SOD activity, and stimulated the upregulation of Keap1, Nrf2, and HO-1 signaling at 72 hours post-ICH. Furthermore, gastrodin significantly increased Bcl-2 expression, while reduced level of Bax, active caspase-3 and active caspase-9, also reduced the number of active caspase-3 or TUNEL positive neurons at 72 hours post-ICH. CONCLUSION: These results suggest that gastrodin is neuroprotective after ICH and the mechanism may be associated with the inhibition of oxidative stress and neuronal apoptosis.

13.
Mikrochim Acta ; 186(12): 778, 2019 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-31728642

RESUMO

Platinum nanoparticles (Pt NPs) covered with a bovine serum albumin scaffold and a particle size of 1.5 nm (BSA-PtS NPs) are shown to display enhanced multiple enzyme-mimicking activities including peroxidase, oxidase, and catalase-like activities. The peroxidase-like activity is characterized by robustness and low signal background. BSA-PtS NPs were used to design colorimetric assays for H2O2 and glucose. H2O2 latter reacts with 3,3',5,5'-tetramethylbenzidine in the presence of BSA-PtS NPs to form a blue product with an absorption maximum at 652 nm. The assay works in the 5-250 µM H2O2 concentration range. The glucose assay is based on its glucose oxidase-catalyzed oxidation to produce gluconic acid and H2O2 which then is colorimetrically quantified. Response is linear in the 10-120 µM glucose concentration range, and the detection limit is 2 µM (at S/N = 3). The method correlates well with the glucose standard method (R2 = 0.997 in the 95% confidence interval) which confirms that glucose in human serum has been successfully detected. Graphical abstractImproved enzymatic assay for hydrogen peroxide and glucose by exploiting the enzyme-mimicking properties of BSA-coated platinum nanoparticles.

14.
Pediatr Blood Cancer ; : e28047, 2019 Nov 17.
Artigo em Inglês | MEDLINE | ID: mdl-31736278

RESUMO

PURPOSE: To estimate the absolute number of adult survivors of childhood cancer in the U.S. population who carry a pathogenic or likely pathogenic variant in a cancer predisposition gene. METHODS: Using the Surveillance, Epidemiology, and End Results (SEER) Program, we estimated the number of childhood cancer survivors on December 31, 2016 for each childhood cancer diagnosis, multiplied this by the proportion of carriers of pathogenic/likely pathogenic variants in the St. Jude Lifetime Cohort (SJLIFE) study, and projected the resulting number onto the U.S. RESULTS: Based on genome sequence data, 11.8% of 2450 SJLIFE participants carry a pathogenic/likely pathogenic variant in one of 156 cancer predisposition genes. Given this information, we estimate that 21 800 adult survivors of childhood cancer in the United States carry a pathogenic/likely pathogenic variant in one of these genes. The highest estimated absolute number of variant carriers are among survivors of central nervous system tumors (n = 4300), particularly astrocytoma (n = 1800) and other gliomas (n = 1700), acute lymphoblastic leukemia (n = 4300), and retinoblastoma (n = 3500). The most frequently mutated genes are RB1 (n = 3000), NF1 (n = 2300), and BRCA2 (n = 800). CONCLUSION: Given the increasing number of childhood cancer survivors in the United States, clinicians should counsel survivors regarding their potential genetic risk, consider referral for genetic counseling and testing, and, as appropriate, implement syndrome-specific cancer surveillance or risk-reducing measures.

15.
Lancet Respir Med ; 2019 Oct 15.
Artigo em Inglês | MEDLINE | ID: mdl-31628085

RESUMO

BACKGROUND: Ensartinib is a potent new-generation ALK inhibitor with high activity against a broad range of known crizotinib-resistant ALK mutations and CNS metastases. We aimed to assess the efficacy and safety of ensartinib in ALK-positive patients with non-small-cell lung cancer (NSCLC), in whom crizotinib therapy was unsuccessful. The associations between ensartinib efficacy and crizotinib-resistant mutations were also explored. METHODS: We did a single-arm, open-label, phase 2 study at 27 centres in China. Patients were aged 18 years or older, had stage IIIb or stage IV ALK-positive NSCLC that had progressed while they were on crizotinib therapy, an Eastern Cooperative Oncology Group performance status of 2 or less, had measurable disease, and had received fewer than three previous treatments. Patients with CNS metastases were included if these metastases were asymptomatic and did not require steroid therapy. All patients received 225 mg ensartinib orally once daily on a continuous dosing schedule. The primary outcome was the proportion of patients with an objective response according to the Response Evaluation Criteria in Solid Tumors (version 1.1), as assessed by an independent review committee in all patients who received at least one dose of ensartinib with no major violations of the inclusion criteria (ie, the full analysis set). Safety was assessed in all enrolled patients who received at least one dose of ensartinib. This trial was registered with ClinicalTrials.gov, NCT03215693. FINDINGS: Between Sept 28, 2017, and April 11, 2018, 160 patients were enrolled and had at least one dose of ensartinib (safety analysis set). Four patients had inclusion violations and were excluded from the efficacy analysis, which thus included 156 patients (full analysis set). 97 (62%) patients in the full analysis set had brain metastases. 76 (52% [95% CI 43-60]) of 147 patients in the full analysis set, with responses that could be assessed by the independent review committee, had an objective response. 28 (70% [53-83]) of 40 patients with measurable brain metastases as assessed by the independent review committee had an intracranial objective response. 145 (91%) of 160 patients had at least one treatment-related adverse event, which were mostly grade 1 or 2. The most common treatment-related adverse events were rash (89 [56%]), increased alanine aminotransferase concentrations (74 [46%]), and increased aspartate aminotransferase concentrations (65 [41%]). INTERPRETATION: Ensartinib has activity and is well tolerated in patients with crizotinib-refractory, ALK-positive NSCLC, including those with brain metastases. The role of ensartinib in patients in whom other second-generation ALK inhibitors have been unsuccessful warrants further studies. FUNDING: Betta Pharmaceuticals.

16.
J Surg Res ; 246: 274-283, 2019 Oct 12.
Artigo em Inglês | MEDLINE | ID: mdl-31614325

RESUMO

BACKGROUND: Fluid therapy influences glycocalyx shedding; however, the effect of this intervention on glycocalyx shedding in patients with glioma remains unclear. In this study, we have investigated glycocalyx shedding and cerebral metabolism during colloid loading in patients with and without glioma. METHODS: Forty patients undergoing general anesthesia were assigned to the glioma brain group (n = 20) or the normal brain group (n = 20); patients in the normal brain group were undergoing partial hepatectomy to treat liver cancer. All patients were subjected to 15 mL/kg hydroxyethyl starch (HES) loading after the induction of anesthesia. Glycocalyx shedding, reflected by syndecan-1 and heparan sulfate levels at the jugular venous bulb, was measured in both groups. We also evaluated cerebral metabolism parameters, including jugular venous oxygen saturation (SjvO2), arterial-jugular venous differences in oxygen (CajvO2), glucose (A-JvGD), lactate (A-JvLD), the cerebral extraction ratio for oxygen (CERO2), and the oxygen-glucose index. RESULTS: Our results showed that patients in the glioma brain group had lower preoperative basal syndecan-1 shedding in plasma than patients in the normal brain group. The hematocrit (Hct)-corrected syndecan-1 level was significantly increased after 15 mL/kg HES fluid administration (19.78 ± 3.83 ng/mL) compared with the Hct-correct baseline syndecan-1 level (15.67 ± 2.35 ng/mL) in patients in the glioma brain group. Similarly, for patients in the normal brain group, Hct-corrected syndecan-1 level was significantly increased after HES loading (34.71 ± 12.83 ng/mL) compared with the baseline syndecan-1 level (26.07 ± 12.52 ng/mL). However, there were no intergroup or intragroup differences in Hct-corrected heparan sulfate levels at any time point. Our study also showed that the SjvO2 was lower and CajvO2 and CERO2 were higher in the glioma brain group at 30 min after HES loading. Intragroup analysis showed that CERO2 and CajvO2 increased after general anesthesia compared with the baseline values in the glioma brain group. In contrast, cerebral metabolism in the normal brain group was unchanged during perioperative period. There were no significant differences in oxygen-glucose index between the two groups throughout the study period. CONCLUSIONS: Preoperative 15 mL/kg HES loading had similar effects on systemic glycocalyx shedding in both the glioma brain and normal brain groups, although patients in the normal brain group had higher levels of plasma syndecan-1. Furthermore, the intraoperative anesthetic management may substantially influence cerebral metabolism in patients with glioma.

17.
Phys Chem Chem Phys ; 21(39): 22057-22066, 2019 Oct 09.
Artigo em Inglês | MEDLINE | ID: mdl-31565723

RESUMO

An X-ray amorphous phase is frequently present at the early stage of calcium phosphate crystallization, and the relevant solution chemistry is essential for understanding the mechanism of reaction. Here, we report a quantitative study of a series of reaction systems at pseudo-equilibrium states. We determined the composition of solutions and the quantities of the precipitate samples, and characterized the long- and short-range order of the precipitate using X-ray diffraction and synchrotron X-ray absorption near-edge structure spectroscopy, respectively. We found that, in a particle with multiple structural units, only a fraction of the units was able to reach pseudo-equilibrium with the solution composition, which represents the average number of surficial clusters per unit. These findings enabled us to propose a general form of the equilibrium constant equation. The equation fits the pseudo-equilibrium data well, and it converts to the "solubility product (Ksp)" and the conventional "reaction quotient" in two limit cases, respectively. Further, using a cube model, we derived a "particle equation" that reveals the connection between the particle structure and the form of equilibrium constant equation. The dependency of the form of pseudo-equilibrium equation on the structure and size of the precipitate reveals a fundamental relation in chemistry, and its applicability remains to be examined in other reaction systems, such as those involving nanocrystals and porous materials.

18.
Radiother Oncol ; 2019 Sep 26.
Artigo em Inglês | MEDLINE | ID: mdl-31564553

RESUMO

PURPOSE: We aimed to determine whether multiple-CT (MCT) optimization of intensity-modulated proton therapy (IMPT) could improve plan robustness to anatomical changes and therefore reduce the additional need for adaptive planning. METHODS AND MATERIALS: Ten patients with head and neck cancer who underwent IMPT were included in this retrospective study. Each patient had primary planning CT (PCT), a first adaptive planning CT (ACT1), and a second adaptive planning CT (ACT2). Selective robust IMPT plans were generated using each CT data set (PCT, ACT1, and ACT2). Moreover, a MCT optimized plan was generated using the PCT and ACT1 data sets together. Dose distributions optimized using each of the four plans (PCT, ACT1, ACT2, and MCT plans) were re-calculated on ACT2 data. The doses to the target and to organs at risk were compared between optimization strategies. RESULTS: MCT plans for all patients met all target dose and organs-at-risk criteria for all three CT data sets. Target dose and organs-at-risk dose for PCT and ACT1 plans re-calculated on ACT2 data set were compromised, indicating the need for adaptive planning on ACT2 if PCT or ACT1 plans were used. The D98% of CTV1 and CTV3 of MCT plan re-calculated on ACT2 were both above the coverage criteria. The CTV2 coverage of the MCT plan re-calculated on ACT2 was worse than ACT2 plan. The MCT plan re-calculated on ACT2 data set had lower chiasm, esophagus, and larynx doses than did PCT, ACT1, or ACT2 plans re-calculated on ACT2 data set. CONCLUSIONS: MCT optimization can improve plan robustness toward anatomical change and may reduce the number of plan adaptation for head and neck cancers.

19.
Bioinformatics ; 2019 Sep 30.
Artigo em Inglês | MEDLINE | ID: mdl-31566663

RESUMO

MOTIVATION: The traditional reads per million normalization method is inappropriate for the evaluation of ChIP-seq data when treatments or mutations have global effects. Changes in global levels of histone modifications can be detected with exogenous reference spike-in controls. However, most ChIP-seq studies overlook the normalization that must be corrected with spike-in. A method that retrospectively renormalizes datasets without spike-in is lacking. RESULTS: ChIPseqSpikeInFree is a novel ChIP-seq normalization method to effectively determine scaling factors for samples across various conditions and treatments, which does not rely on exogenous spike-in chromatin or peak detection to reveal global changes in histone modification occupancy. Application of ChIPseqSpikeInFree on five datasets demonstrates that this in silico approach reveals a similar magnitude of global changes as the spike-in method does. AVAILABILITY AND IMPLEMENTATION: St Jude Cloud (https://pecan.stjude.cloud/permalink/spikefree) and St. Jude Github ( https://github.com/stjude/ChIPseqSpikeInFree). SUPPLEMENTARY INFORMATION: Supplementary data are available at Bioinformatics online.

20.
Artigo em Inglês | MEDLINE | ID: mdl-31633848

RESUMO

FeN4 moieties embedded in partially graphitized carbon are the most efficient platinum group metal free active sites for the oxygen reduction reaction in acidic proton-exchange membrane fuel cells. However, their formation mechanisms have remained elusive for decades because the Fe-N bond formation process always convolutes with uncontrolled carbonization and nitrogen doping during high-temperature treatment. Here, we elucidate the FeN4 site formation mechanisms through hosting Fe ions into a nitrogen-doped carbon followed by a controlled thermal activation. Among the studied hosts, the ZIF-8-derived nitrogen-doped carbon is an ideal model with well-defined nitrogen doping and porosity. This approach is able to deconvolute Fe-N bond formation from complex carbonization and nitrogen doping, which correlates Fe-N bond properties with the activity and stability of FeN4 sites as a function of the thermal activation temperature.

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