急性主动脉夹层发生低氧血症患者危险因素的Meta分析

目的通过Meta分析明确主动脉夹层患者发生低氧血症的危险因素。方法检索中英文数据库及纳入文献的参考文献,由2位评价人员按照标准独立筛选文献,提取资料并进行文献质量评价,应用RevMan5.0分析软件对资料进行Meta分析。结果从27篇文献筛选7篇符合纳入标准,样本量为1175例,主动脉夹层发生低氧血症患者为376例,主动脉夹层发生非低氧血症患者为799例,共纳入危险因素63个,仅体重指数(BMI)>25kg/m^2、动脉血氧分压/吸人氧浓度(PaO_2/FiO_2)≤300mmHg、体外循坏时间、机械通气延长、ICU留置时间合并效应量差异有统计学意义,是主动脉夹层发生低氧血症的预测因素;介入治疗是主动脉夹层的保护因素。结论该研究表明,BMI>25kg/m^2、PaO_2/FiO_2≤300mmHg、体外循坏时间、机械通气延长、ICU留置时间是主动脉夹层并发低氧血症的危险因素。术后低氧血症是主动脉夹层的常见并发症,其危险因素受多种因素的影响,仍需更大量前瞻性、高质量的研究进行分析。

IDMs合并心肌损害对GPBB的影响及其意义

目的研究糖原磷酸化酶同功酶脑型(GPBB)在糖尿病母亲婴儿(IDMs)合并心肌损害时的变化及其意义。方法选取2014年1月-2014年12月于河北大学附属医院入住新生儿病房的132例IDMS为研究对象,于出生后3、6、12和24 h分别检测血清GPBB浓度。比较无心肌损害组、心肌损害组及对照组各时间点GPBB的水平变化,分析GPBB与围产高危因素的关系。结果心肌损害组血清GPBB水平高于无心肌损害组和对照组(P<0.05)。母亲孕期血糖控制不良、妊娠期糖尿病病程长(≥3个月)、新生儿低血糖对GPBB水平的影响较大(P<0.05)。结论 GPBB可作为检测IDMs发生心肌损害的早期敏感指标。

Mutations of beta-amyloid precursor protein alter the consequence of Alzheimer's disease pathogenesis

Alzheimer's disease is pathologically defined by accumulation of extracellular amyloid-β(Aβ). Approximately 25 mutations in β-amyloid precursor protein(APP) are pathogenic and cause autosomal dominant Alzheimer's disease. To date, the mechanism underlying the effect of APP mutation on Aβ generation is unclear. Therefore, investigating the mechanism of APP mutation on Alzheimer's disease may help understanding of disease pathogenesis. Thus, APP mutations(A673T, A673 V, E682 K, E693 G, and E693Q) were transiently co-transfected into human embryonic kidney cells. Western blot assay was used to detect expression levels of APP, beta-secretase 1, and presenilin 1 in cells. Enzyme-linked immunosorbent assay was performed to determine Aβ_(1–40) and Aβ_(1–42) levels. Liquid chromatography-tandem mass chromatography was used to examine VVIAT, FLF, ITL, VIV, IAT, VIT, TVI, and VVIA peptide levels. Immunofluorescence staining was performed to measure APP and early endosome antigen 1 immunoreactivity. Our results show that the protective A673 T mutation decreases Aβ_(42)/Aβ_(40) rate by downregulating IAT and upregulating VVIA levels. Pathogenic A673 V, E682 K, and E693 Q mutations promote Aβ_(42)/Aβ_(40) rate by increasing levels of CTF99, Aβ_(42), Aβ_(40), and IAT, and decreasing VVIA levels. Pathogenic E693 G mutation shows no significant change in Aβ_(42)/Aβ_(40) ratio because of inhibition of γ-secretase activity. APP mutations can change location from the cell surface to early endosomes. Our findings confirm that certain APP mutations accelerate Aβ generation by affecting the long Aβ cleavage pathway and increasing Aβ_(42/40) rate, thereby resulting in Alzheimer's disease.

Baculoviral inhibitor of apoptosis protein repeatcontaining protein 3 delays early Wallerian degeneration after sciatic nerve injury

Wallerian degeneration is a complex biological process that occurs after nerve injury,and involves nerve degeneration and regeneration.Schwann cells play a crucial role in the cellular and molecular events of Wallerian degeneration of the peripheral nervous system.However,Wallerian degeneration regulating nerve injury and repair remains largely unknown,especially the early response.We have previously reported some key regulators of Wallerian degeneration after sciatic nerve injury.Baculoviral inhibitor of apoptosis protein repeat-containing protein 3(BIRC3)is an important factor that regulates apoptosis-inhibiting protein.In this study,we established rat models of right sciatic nerve injury.In vitro Schwann cell models were also established and subjected to gene transfection to inhibit and overexpress BIRC3.The data indicated that BIRC3 expression was significantly up-regulated after sciatic nerve injury.Both BIRC3 upregulation and downregulation affected the migration,proliferation and apoptosis of Schwan cells and affected the expression of related factors through activating c-fos and ERK signal pathway.Inhibition of BIRC3 delayed early Wallerian degeneration through inhibiting the apoptosis of Schwann cells after sciatic nerve injury.These findings suggest that BIRC3 plays an important role in peripheral nerve injury repair and regeneration.The study was approved by the Institutional Animal Care and Use Committee of Nantong University,China(approval No.2019-nsfc004)on March 1,2019.

Effect and mechanism of baicalin and geniposide on excitotoxicity of acute cerebral ischemia

OBJECTIVE Based on the methods of microdialysis,HPLC-MS/MS and gene chip tech.nology,the mechanism of Baicalin and Geniposide(BC/GP) against excitatory amino acid toxicity in ce.rebral ischemia was studied.This will provide guidance for the clinical application of BC/GP and the study of excitatory amino acid toxicity in cerebral ischemia.METHODS(1) Microdialysis technique and HPLC-MS/MS was performed to study the pharmacodynamics of BC/GP against cerebral ischemia.(1)18 SD rats with body weight of(280±20) g were randomly divided into control group,treatment groups with BC/CP at low dose,medium dose and high dose(equal to the dosage of crude drugs for 30 mg·kg^(-1),45 mg·kg^(-1) and 60 mg·kg^(-1) respectively).Rats in each group were given intragastric administration for seven days to establish cerebral ischemia model.Then,microdialysis probe was applied to collect cerebrospinal fluid from hippocampus before and after cerebral ischemia.(2) First,we established the HPLC-MS/MS method for measuring drugs and excitatory amino acids.Then we detected the microdi.alysis samples and observed their changes in animals.(2) The mechanism of BC/GP against excitatory toxicity of cerebral ischemia were observed at gene level by chip technique.(1) 16 SD rats with body weight of 240±20 g were randomly divided into sham group,model group,treatment group of BC(60 mg·kg^(-1)),treatment group of GP(60 mg·kg^(-1)) and treatment group of BC/GP(7:3)(60 mg·kg^(-1)).Rats in eachgroup were given intragastric administration for seven days to establish cerebral ischemia model.Then the rats were sacrificed,and the hippocampus were rapidly harvested and stored at-80℃ for further detection.(2) After the quality inspection of the hippocampal,the qualified samples were subjected to detect the levels of neurotransmitter receptor gene in the ischemic of rats by gene chip technology.Finally,the results were analyzed by the method of ΔΔCt.RESULTS(1) Only three compounds includ.ed GP,glutamic acid and aspartic acid were detected in microdialysis samples by HPLC-MS/MS.The concentration of GP increased and lasted for 120 min with a significant dose-dependent after cerebral ischemia.Compared with low dose group,the AUC(0-t),MRT(0-∞),Cmax and t1/2 z in high-dose group showed significant difference(P<0.01).Compared with the model group,the levels of glutamic acid and aspartic acid in the treatment groups decreased significantly,especially in the middle and high dose groups.(2)89 genes in the neurotransmitter receptor gene signaling pathway were detected by gene chip technol.ogy.There were 22 genes with |Fold Regulation| >1.5 in the model group,compared with the sham group.Five of the 22 genes showed statistically significant differences,including Grin2 c(2.9026),Chrna7(-1.5877),and Tacr2(-1.7695).Htr3 a(-1.8172) and Grm6(-2.3527).There were 5 genes with |Fold Regulation|>1.5 in the BC group,compared with the model group,Two of them exhibited statistically significant differences,including Brs3(1.797)and Grin2 c(-1.7979).There were 14 genes with |Fold Reg.ulation| >1.5 in the GP group,compared with the model group.Three of them displayed statistically significant differences,including Hcrtr2(-1.6584),Sctr(-3.8524) and Grin2 c(-4.8408).Compared with model group,the genes of |Fold Regulation| >1.5 in BC/GP(7:3) group are 5,and only one of them showed a significant differences.CONCLUSION(1) After administration of BC and GP,GP can cross the blood-brain barrier and reduce the release of excitatory amino acids in the hippocampus.(2) BC/GP can inhibit the interaction between excitatory amino acids and excitatory amino acid receptors and attenuate the toxicity of excitatory amino acids by down-regulating the expression of glutamic acid receptor Grin2 c gene.(3) BC/GP may exert their brain protection effect by reducing the release of excit.atory amino acids and inhibiting the expression of excitatory amino acid receptors.

Interfacial active sites on Co-Co_(2)C@carbon heterostructure for enhanced catalytic hydrogen generation

Designing catalysts with capable dual-active sites to drive catalytic hydrogen generation is necessary for the future hydrogen economy.Herein,the interfacial active sites consisting of Co and Co-C on Co-Co_(2)C@carbon heterostructure are designed through annealing and highpressure carbonization.The operating temperature during the high-pressure carbonization under a CO-reducing environment is responsible for the construction and regulation of Co-Co_(2)C@C heterostructure.The optimal catalyst has a high turnover frequency(TOF) of33.1 min^(-1) and low activation energy(E_a) of27.3 kJ-mol^(-1) during the hydrolysis of NH_(3)BH_(3).The catalytic stability of Co-Co_(2)C@C has no dramatic deterioration even after 5 cyclic usages.The interfacial active sites and the carbon on the catalyst surface enhance hydrogen generation kinetics and catalytic stability.The construction of interfacial active sites in Co-Co_(2)C@C prompts the dissociation of reactants(NH_(3)BH_(3) and H_(2)O molecules),leading to an enhanced catalytic hydrogen generation from NH_(3)BH_(3) hydrolysis(Co activates NH_(3)BH_(3) and Co-C activates H_(2)O).The construction of hetero-structural catalysts provides theoretical direction for the rational design of advanced transition metal carbide materials in the field of energy catalysis and conversion.

利用薄膜去润湿行为研究线形和环形聚苯乙烯及共混薄膜的黏度

研究了线形聚苯乙烯(LPS)薄膜,环形聚苯乙烯(RPS)薄膜以及不同配比的共混薄膜在聚二甲基硅氧烷(PDMS)高分子刷上的去润湿动力学行为.研究发现,LPS薄膜的去润湿速度要快于RPS薄膜的去润湿速度,共混薄膜的去润湿速度介于LPS薄膜和RPS薄膜之间,且共混薄膜的去润湿速度随着RPS在共混薄膜中含量的增加而降低.利用水和乙二醇在薄膜表面的接触角计算得到LPS薄膜,RPS薄膜及共混薄膜的表面张力.结果发现,共混薄膜的表面张力均小于LPS薄膜和RPS薄膜的表面张力,且当RPS含量为70%时,共混薄膜的表面张力达到最小值.通过对薄膜在去润湿过程中的孔半径、去润湿速度、边宽以及后退接触角的研究,获得了LPS薄膜、RPS薄膜及共混薄膜的黏度.结果表明,LPS薄膜的黏度要低于RPS薄膜的黏度,实验得到的不同比例共混薄膜的黏度介于LPS薄膜和RPS薄膜的黏度之间,且其低于LPS和RPS的质量权重平均值.

Rheological Properties of Waterborne Polyurethane Paints

The rheological properties of two specific waterborne polyurethane （PU） paints were studied by both macrorheological and microrheological methods. During the macrorheological measurement on a rotary rheometer, evaporation of solvent cannot be totally excluded, which has an influence on the reliability of rheological results. So, the linear oscillatory frequency sweep results （storage and loss modulus versus frequency） and steady shear results （viscosity versus shear rate） got from the rotary rheometer measurement are only used for qualitative analysis. As the evaporation of solvent can be neglected during microrheological measurements on a diffusing wave spectroscope （DWS）, the results of storage modulus （G3 and loss modulus （G＇~） versus frequency are more credible than the results obtained from the rotary rheometer measurement. Thus, the results of G＇ and G＂ versus frequency from DWS measurements are used for quantitative analysis in this work. The G＇ for both of the waterborne PU paints are larger than G＂ at low frequency and that is opposite at high frequency in the experimental angular frequency range. The values of modulus at same frequency and viscosity at low shear rate for the two PU paints have apparent difference, which determines the difference of their application.

Dewetting Kinetics of Thin Polymer Films with Different Architectures:Effect of Polymer Adsorption

We have investigated the influence of the adsorption process on the dewetting behavior of the linear polystyrene film （LPS）, the 3-arm star polystyrene film （3SPS） and the ring polystyrene film （RPS） on the silanized Si substrate. Results show that the adsorption process greatly influences the dewetting behavior of the thin polymer films. On the silanized Si substrate, the 3SPS chains exhibit stronger adsorption compared with the LPS chains and RPS chains; as a result, the wetting layer forms more easily. For LPS films, with the decrease of annealing temperature, the kinetics of polymer film changes from exponential behavior to slip dewetting. As a comparison, the stability of 3SPS and RPS films switches from slip dewetting to unusual dewetting kinetic behavior. The adsorbed nanodroplets on the solid substrate play an important role in the dewetting kinetics by reducing the driving force of dewetting and increase the resistant force of dewetting. Additionally, Brownian dynamics （BD） simulation shows that the absolute values of adsorption energy （ε） gradually increase from linear polymer （-0.3896） to ring polymer （-0.4033） and to star polymer （-0.4264）, which is consistent with the results of our adsorption experiments.

Scalable synthesis of mesoporous FeS_(2) nanorods as highperformance anode materials for sodium-ion batteries

Sodium-ion batteries(SIBs),as highly promising alternatives to lithium-ion batteries(LIBs),can be widely used in a variety of next-generation energy storage systems.However,the current commercial graphite anodes of LIBs could not intercalate sodium ions to appreciable extent,and the electrochemical irreversibility hinders further application.Searching for a suitable anode material is a critical issue for the successful development of SIBs.Herein,we report a convenient,fast,and large-scale preparation method of mesoporous FeS_(2) nanorods.Our specially designed one-dimensional mesoporous structure of FeS_(2) takes full advantage of ultra-high strain relaxation as well as fast Na^(+)transport rate arising from microstructural characteristics.As a result,the mesoporous FeS_(2) nanorods exhibited excellent sodium storage performance.The discharge capacity was retained at 711.1 mAh·g^(-1) after 450 cycles at a current density of 1000 mA·g^(-1).The special microstructure and superior performance of mesoporous FeS_(2) nanorods represent a critical step for transition metal sulfides electrode materials toward practical SIBs application.

Claudin 14/15 play important roles in early wallerian degeneration after rat sciatic nerve injury

Purpose:Wallerian degeneration(WD)is an antegrade degenerative process distal to peripheral nerve injury.Numerous genes are differentially regulated in response to the process.However,the underlying mechanism is unclear,especially the early response.We aimed at investigating the effects of sciatic nerve injury on WD via CLDN 14/15 interactionsin vivo andin vitro.Methods:Using the methods of molecular biology and bioinformatics analysis,we investigated the molecular mechanism by which claudin 14/15 participate in WD.Our previous study showed that claudins 14 and 15 trigger the early signal flow and pathway in damaged sciatic nerves.Here,we report the effects of the interaction between claudin 14 and claudin 15 on nerve degeneration and regeneration during early WD.Results:It was found that claudin 14/15 were upregulated in the sciatic nerve in WD.Claudin 14/15 promoted Schwann cell proliferation,migration and anti-apoptosisin vitro.PKCα,NT3,NF2,and bFGF were significantly upregulated in transfected Schwann cells.Moreover,the expression levels of theβ-catenin,p-AKT/AKT,p-c-jun/c-jun,and p-ERK/ERK signaling pathways were also significantly altered.Conclusion:Claudin 14/15 affect Schwann cell proliferation,migration,and anti-apoptosis via theβ-catenin,p-AKT/AKT,p-c-jun/c-jun,and p-ERK/ERK pathwaysin vitro andin vivo.The results of this study may help elucidate the molecular mechanisms of the tight junction signaling pathway underlying peripheral nerve degeneration.