An effective'salt in dimethyl sulfoxide/water'electrolyte enables high-voltage supercapacitor operated at-50℃

Compared with organic electrolytes,aqueous electrolytes exhibit significantly higher ionic conductivity and possess inherent safety features,showcasing unique advantages in supercapacitors.However,challenges remain for low-salt aqueous electrolytes operating at high voltage and low temperature.Herein,we report a low-salt(0.87 m,m means mol kg^(-1))'salt in dimethyl sulfoxide/water'hybrid electrolyte with non-flammability via hybridizing aqueous electrolyte with an organic co-solvent of dimethyl sulfoxide(hydrogen bond acceptor).As a result,the 0.87 m hybrid electrolyte exhibits enhanced electrochemical stability,a freezing temperature below-50℃,and an outstanding ionic conductivity of 0.52mS cm~(-1)at-50℃.Dimethyl sulfoxide can anchor water molecules through intermolecular hydrogen bond interaction,effectively reinforcing the stability of water in the hybrid electrolyte.Furthermore,the interaction between dimethyl sulfoxide and water molecules diminishes the involvement of water in the generation of ordered ice crystals,finally facilitating the low-temperature performance of the hybrid electrolyte.When paired with the 0.87 m'salt in dimethyl sulfoxide/water'hybrid electrolyte,the symmetric supercapacitor presents a 2.0 V high operating voltage at 25℃,and can operate stably at-50℃.Importantly,the suppressed electrochemical reaction of water at-50℃further leads to the symmetric supercapacitor operated at a higher voltage of 2.6 V.This modification strategy opens an effective avenue to develop low-salt electrolytes for high-voltage and low-temperature aqueous supercapacitors.

Dimethyl sulfoxide inhibits zymosan-induced intestinal inflammation and barrier dysfunction

AIM: To investigate whether dimethyl sulfoxide(DMSO) inhibits gut inflammation and barrier dysfunction following zymosan-induced systemic inflammatoryresponse syndrome and multiple organ dysfunction syndrome.METHODS: Sprague-Dawley rats were randomly divided into four groups: sham with administration of normal saline(SS group); sham with administration of DMSO(SD group); zymosan with administration of normal saline(ZS group); and zymosan with administration of DMSO(ZD group). Each group contained three subgroups according to 4 h,8 h,and 24 h after surgery. At 4 h,8 h,and 24 h after intraperitoneal injection of zymosan(750 mg/kg),the levels of intestinal inflammatory cytokines [tumor necrosis factor-alpha(TNF-α) and interleukin(IL)-10] and oxides(myeloperoxidase,malonaldehyde,and superoxide dismutase) were examined. The levels of diamine oxidase(DAO) in plasma and intestinal mucosal blood flow(IMBF) were determined. Intestinal injury was also evaluated using an intestinal histological score and apoptosis of intestinal epithelial cells was determined by deoxynucleotidyl transferase d UTP nick end labeling(TUNEL) assay. The intestinal epithelial tight junction protein,ZO-1,was observed by immunofluorescence.RESULTS: DMSO decreased TNF-α and increased IL-10 levels in the intestine compared with the ZS group at the corresponding time points. The activity of intestinal myeloperoxidase in the ZS group was higher than that in the ZD group 24 h after zymosan administration(P < 0.05). DMSO decreased the content of malondialdehyde(MDA) and increased the activity of superoxide dehydrogenase(SOD) 24 h after zymosan administration. The IMBF was lowest at 24 h and was 49.34% and 58.26% in the ZS group and ZD group,respectively(P < 0.05). DMSO alleviated injury in intestinal villi,and the gut injury score was significantly lower than the ZS group(3.6 ± 0.2 vs 4.2 ± 0.3,P < 0.05). DMSO decreased the level of DAO in plasma compared with the ZS group(65.1 ± 4.7 U/L vs 81.1 ± 5.0 U/L,P < 0.05). DMSO significantly preserved ZO-1 protein expression and localization 24 h after zymosan administration. The TUNEL analysis indicated that the number of apoptotic intestinal cells in the ZS group was much higher than the ZD group(P < 0.05).CONCLUSION: DMSO inhibited intestinal cytokines and protected against zymosan-induced gut barrier dysfunction.

Excess properties and spectroscopic studies for binary system polyethylene glycol 600 + dimethyl sulfoxide at T =(298.15, 303.15,308.15, 313.15, and 318.15) K

The work presents density(ρ) and viscosity(η) data of binary system polyethylene glycol 600(PEG) + dimethyl sulfoxide(DMSO) over the entire concentration range at T =(298.15, 303.15, 308.15, 313.15 and 318.15) K and atmospheric pressure. On the basis of density and viscosity values, the excess properties of PEG(1) + DMSO(2) mixtures, including excess molar volume(V_m^E), viscosity deviation(Δη), excess free energies of activation(ΔG^(*E)), and isobaric thermal expansion coefficient(αp), were calculated. At the same time, in order to conjecture the density viscosity under different conditions, the density and viscosity data were fitted with the corresponding formula. The calculated results of V_m^E, Δη, and ΔG^(*E) were fitted with the Redlich–Kister equation to derive coefficients and estimate the standard deviations(σ) between the experimental and calculated values. Moreover, the intermolecular interaction of PEG with DMSO was discussed on the basis of FTIR and UV–Vis spectral results of PEG(1) + DMSO(2) mixtures. The results indicated that there were the hydrogen bonding and interactions of hydroxyl hydrogen atoms in PEG with oxygen atoms in DMSO.

Synthesis and Crystal Structure of [(Praseodymium)_2(3,5-Binitro Benzoyloxy)_6 (Dimethyl Sulfoxide)_4] Complex

A novel one-dimensional chain complex [Pr2(bnbo)6(DMSO)4] (bnbo=3,5-binitro benzoyloxy, DMSO= dimethyl sulfoxide) with bridging carboxyl groups was synthesized and its structure has been determined by single-crystal X-ray methods. In the complex, a pair of adjacent metal ions are alternately connected by four or two carboxylate groups to form an infinite chain of 8-coordinated Pr3+ ions. The complex (Pr2C50H42N12O40S4 ) crystal system is triclinic, with space group P1, a=14.2890(3), b=14.3427(3), c=20.1601(2)? =76.636(1), b=84.496(1), =60.316(1)? V=3491.4(1)?, Z=2, Mr =1861.02, Dc=1.770 g/cm3, m=1.608mm-1, F(000)=1856, the final R=0.0776 and wR=0.1724 for 8804 reflections with I > 2s(I).

DMSO诱导HL60细胞分化过程中的吞噬和杀伤功能

目的探究HL60分化过程中吞噬和杀伤的功能变化。方法本研究首先使用流式细胞术和髓系过氧化物酶(MPO)检测方法监测二甲亚砜(DMSO)诱导HL60细胞的成熟过程。接着利用金黄色葡萄球菌体外感染实验分析了此过程中细胞的吞噬和杀伤功能变化。结果CD11b的表达随诱导时间延长而升高,到第8天达到高峰,MPO表达量显著下降,6 d以后达到最低。DMSO诱导HL60细胞后第4天达到最佳吞噬和杀伤效果。结论HL60经DMSO诱导后,吞噬和杀伤功能的变化与类中性粒细胞成熟过程并不完全一致。这为DMSO诱导的HL60细胞在吞噬和杀伤实验的应用提供了参考。

Innovate combination of sevoflurane dilution in dimethyl sulfoxide: A stability study by gas chromatography and nuclear magnetic resonance

To investigate physicochemical stability of sevofuranein dimethyl sulfoxide using gas chromatography with a fame ionization detector and nuclear magnetic reso-nance （NMR）.METHODSUndiluted sevoflurane, plus dilutions 1：2, 1：5, 1：10, 1：25, and 1：50 in dimethyl sulfoxide were prepared in a vertical laminar fow cabinet class Ⅱ type B and stored at different temperatures （23 ℃, 6 ℃, and -10 ℃） for 45 d. Sterile 1 mL polypropylene amber syringes to minimize light degradation, caps and needles were used. The presence of sevofurane and its degradation products in the samples was determined by gas chroma-tography with flame ionization detector （260 ℃, 40min）, and by 1H, 19F, and proton-decoupled 19F nuclearmagnetic resonance.RESULTS The gas chromatography analysis showed sevofluraneand dimethyl sulfoxide （DMSO） retention times were 2.7and 13.0 min, respectively. Pure DMSO injection into thecolumn resulted in two additional peaks at 2.1 and 2.8min. The same sevofurane peak at 2.7 min was observedin all the dilutions at -10 ℃, 4 ℃ and 25 ℃. The NMRspectra showed signals consistent with the sevoflurane structure in all the dilutions at -10 ℃, 4 ℃ and 25 ℃. In the 1H spectrum, two signals corresponding to the sevoflurane molecule were observed at 5.12 and 4.16 parts per million （ppm5）. In the 19F-NMR spectrum, two signals were observed at -76.77 ppm and -157.13 ppm. In the 19F NMR CPD, two signals were observed at -76.77 ppm and -157.13 ppm. The first one showed a doublet （JF-F = 3.1 Hz） which integrated by six fluorine nuclei from the hexafluoro-isopropyl group. The second signal was integrated by a fuorine atom and showed a septuplet （JF-F = 3.1 Hz）.CONCLUSIONThis study shows that different concentrations ofsevofurane in dimethyl sulfoxide retain their chemicalcomposition after exposure to different temperaturesfor a period of 45 d.

Inhibition of matrix metalloproteinase-9 secretion by dimethyl sulfoxide and cyclic adenosine monophosphate in human monocytes

BACKGROUND Matrix metalloproteinases(MMPs),including MMP-9,are an integral part of the immune response and are upregulated in response to a variety of stimuli.New details continue to emerge concerning the mechanistic and regulatory pathways that mediate MMP-9 secretion.There is significant evidence for regulation of inflammation by dimethyl sulfoxide(DMSO)and 3',5'-cyclic adenosine monophosphate(cAMP),thus investigation of how these two molecules may regulate both MMP-9 and tumor necrosis factorα(TNFα)secretion by human monocytes was of high interest.The hypothesis tested in this study was that DMSO and cAMP regulate MMP-9 and TNFαsecretion by distinct mechanisms.AIM To investigate the regulation of lipopolysaccharide(LPS)-stimulated MMP-9 and tumor necrosis factorαsecretion in THP-1 human monocytes by dimethyl sulfoxide and cAMP.METHODS The paper describes a basic research study using THP-1 human monocyte cells.All experiments were conducted at the University of Missouri-St.Louis in the Department of Chemistry and Biochemistry.Human monocyte cells were grown,cultured,and prepared for experiments in the University of Missouri-St.Louis Cell Culture Facility as per accepted guidelines.Cells were treated with LPS for selected exposure times and the conditioned medium was collected for analysis of MMP-9 and TNFαproduction.Inhibitors including DMSO,cAMP regulators,and anti-TNFαantibody were added to the cells prior to LPS treatment.MMP-9 secretion was analyzed by gel electrophoresis/western blot and quantitated by ImageJ software.TNFαsecretion was analyzed by enzyme-linked immuno sorbent assay.All data is presented as the average and standard error for at least 3 trials.Statistical analysis was done using a two-tailed paired Student t-test.P values less than 0.05 were considered significant and designated as such in the Figures.LPS and cAMP regulators were from Sigma-Aldrich,MMP-9 standard and antibody and TNFαantibodies were from R&D Systems,and amyloid-βpeptide was from rPeptide.RESULTS In our investigation of MMP-9 secretion from THP-1 human monocytes,we made the following findings.Inclusion of DMSO in the cell treatment inhibited LPSinduced MMP-9,but not TNFα,secretion.Inclusion of DMSO in the cell treatment at different concentrations inhibited LPS-induced MMP-9 secretion in a dosedependent fashion.A cell-permeable cAMP analog,dibutyryl cAMP,inhibited both LPS-induced MMP-9 and TNFαsecretion.Pretreatment of the cells with the adenylyl cyclase activator forskolin inhibited LPS-induced MMP-9 and TNFαsecretion.Pretreatment of the cells with the general cAMP phosphodiesterase inhibitor IBMX reduced LPS-induced MMP-9 and TNFαin a dose-dependent fashion.Pre-treatment of monocytes with an anti-TNFαantibody blocked LPSinduced MMP-9 and TNFαsecretion.Amyloid-βpeptide induced MMP-9 secretion,which occurred much later than TNFαsecretion.The latter two findings strongly suggested an upstream role for TNFαin mediating LPS-stimulate MMP-9 secretion.CONCLUSION The cumulative data indicated that MMP-9 secretion was a distinct process from TNFαsecretion and occurred downstream.First,DMSO inhibited MMP-9,but not TNFα,suggesting that the MMP-9 secretion process was selectively altered.Second,cAMP inhibited both MMP-9 and TNFαwith a similar potency,but at different monocyte cell exposure time points.The pattern of cAMP inhibition for these two molecules suggested that MMP-9 secretion lies downstream of TNFαand that TNFαmay a key component of the pathway leading to MMP-9 secretion.This temporal relationship fit a model whereby early TNFαsecretion directly led to later MMP-9 secretion.Lastly,antibody-blocking of TNFαdiminished MMP-9 secretion,suggesting a direct link between TNFαsecretion and MMP-9 secretion.

LYOTROPIC AND THERMOTROPIC LIQUID CRYSTALL INE TRIALKYL CELLULOSES OBTAINED DIRECTLY FROM CELLULOSE ACETATE IN DIMETHYL SULFOXIDE

Highly substituted n-atkyl celluloses with sidechains 3 to 10 carbon atoms long have been prepared from cellulose acetate, sodium hydroxide and n-alkyl bromides with dimethyl sulfoxide as solvent. Synthetic conditions of n-alkyl celluloses were studied with respect to reaction temperature, time and yield. The molecular structure of the n-alkyl celluloses, which were obtained as white powders or as sticky, soft and birefringent solids at room temperature, was investigated by IR and NMR spectra and elemental analysis. The highly substituted n-alkyl celluloses all exhibited both therotropic and lyotropic liquid crystalline cholesteric phases in some non-polar solvents. The metting behavior and solubility of the n-alkyl celluloses were examined.

DMSO和As_2O_3对人食管癌细胞增殖的抑制作用

目的 抑制肿瘤细胞生长是治疗肿瘤的重要基础。本文比较二甲基亚砜（ＤＭＳＯ）、三氧化二砷（Ａｓ２Ｏ３）和维甲酸对人食管癌细胞生长抑制的影响。方法 用生长曲线、剂量－效应曲线、＾３Ｈ－ＴｄＲ掺入、ＭＴＴ比色分析、细胞周期的流式术检测、ＰＣＮＡ及Ｃｙｃｌｉｎ Ｄ１免疫组化等多项指标反映细胞增殖改变。结果 二甲基亚砜和三氧化二砷对食管癌细胞株生长的抑制作用较传统的维甲酸效果更强。结论

三种氨基酸从水到DMSO水溶液的迁移焓研究

用微量量热法测定甘氨酸、L-丙氨酸、L-丝氨酸在二甲基亚砜(DMSO)水溶液中的溶解焓,计算得到三种氨基酸从水到DMSO水溶液的迁移焓,根据共球交盖模型对氨基酸与DMSO在水溶液中的相互作用进行讨论,并与前期的氨基酸在尿素水溶液体系中的迁移焓进行比较.结果显示,氨基酸与共溶剂分子之间产生的静电相互作用以及亲水-亲水相互作用对氨基酸迁移焓有负贡献,而亲水-疏水、疏水-疏水相互作用对氨基酸迁移焓有正贡献.与尿素水溶液中氨基酸迁移焓的绝对值随尿素浓度的增加而增加,并规律性地出现多个变化点的情况不同,氨基酸从水到DMSO水溶液的迁移焓随DMSO浓度的增加而线性增加.这种差异反映了尿素与DMSO及其水溶液结构的不同,为认识尿素在水溶液中的缔合作用提供了对比依据.

高岭石-DMSO插层复合物的制备与表征

制备并表征高岭石-二甲基亚砜插层复合物,讨论二甲基亚砜与水的体积比、插层时间和插层温度对插层反应的影响.实验结果表明:二甲基亚砜(DMSO)可以很容易地直接插入高岭石层间,使高岭石的层间距由0.695 0 nm增加到1.085 1 nm;采用超细粉碎高岭石可以大幅度降低DMSO的浓度,提高插层率,如果反应条件控制得当,插层率可达99%以上.红外光谱分析表明,DMSO与高岭石的内表面羟基和内羟基都形成了氢键.扫描电镜显示,高岭石的片状结构因为插层作用的影响在一定程度上受到破坏.

PAN/DMSO溶液的挤出对初生纤维结构的影响

应用扫描电子显微镜（SEM）和x射线衍射仪（XRD）研究了在一定的凝固条件下，挤出剪切速率（γ）对聚丙烯腈（PAN）初生纤维聚集态及形态结构的影响规律。结果表明：随着γ的增加，初生纤维的结晶度增大，晶粒尺寸减小；初生纤维的表面上产生了沿着轴向分布的沟槽，γ越高，沟槽越深，初生纤维的截面结构变得不均匀，出现了一些大孔和皮芯结构；随着γ的增加；初生纤维中的二甲基亚砜（DMSO）残留量增加。控制γ在11721—14651s-1，PAN／DMSO溶液流动性能好，可获得表面沟槽均匀、缺陷少、晶粒尺寸小且结晶度高的结构致密的PAN初生纤维。

贫铀诱发细胞超微结构改变及DMSO的保护作用

目的观察贫铀(DU)对体外培养的人支气管上皮细胞超微结构的影响及二甲基亚砜(DMSO)的保护作用。方法DU作用人支气管上皮细胞(BEAS-2B)24 h后,用荧光染色法检测细胞存活率、坏死率和凋亡率,用透射电子显微镜(TEM)观察细胞超微结构改变。结果荧光显微分析表明,DU作用后,存活细胞数明显减少,凋亡和坏死细胞数显著增高,而DMSO对DU诱发的细胞凋亡和坏死有明显的保护作用。TEM显示,正常细胞和DMSO对照细胞整体形态、核质比例、各种细胞器及细胞骨架均结构清晰;DU处理的细胞,无论细胞内、外有无贫铀颗粒,均见细胞不同程度的凋亡或坏死,正常细胞结构改变或消失,特别是细胞内或外有DU颗粒的细胞,膜性细胞器改变明显,其他细胞器也观察到结构不清或空泡化;DMSO+DU组,即使细胞内外有贫铀分布,各种细胞器结构的改变也明显减轻,观察到有些线粒体、内质网等膜性结构发生膨胀,但细胞整体结构仍较清晰。结论DU可诱发细胞凋亡和坏死,并导致细胞超微结构改变,DMSO对DU所致细胞损伤有明显的保护效果。

DMSO诱导MCF-7细胞凋亡的研究

目的研究二甲基亚砜(DMSO)对MCF-7细胞凋亡的诱导作用。方法用不同浓度DMSO处理体外培养的MCF-7细胞,应用倒置光显微镜观察细胞形态学变化,用MTT比色法检测细胞存活率;Hoechst33258/PI荧光染色,用荧光显微镜分析凋亡细胞比率;琼脂糖凝胶电泳检测DNA梯状条带。结果在倒置光学显微镜下观察1%DMSO处理细胞12h后细胞形态发生变化。约有50%以上的细胞变圆,细胞内有多泡小体形成。随DMSO浓度增加和作用时间的延长,细胞存活率明显下降,经MTT检测其IC_(50)值为1%;荧光显微镜下可见60%以上细胞核染色质凝集,核碎裂等凋亡细胞的形态学变化;琼脂糖凝胶电泳呈现梯状条带(DNA ladder)。结论适当浓度的DMSO能够抑制乳腺癌细胞增殖并诱导其凋亡。

DMSO、DMF和H_2O体系相平衡数据的测定和预测

采用拟静态沸点仪法测定了二元体系二甲基亚砜(DMSO)-N,N-二甲基甲酰胺(DMF)、DMSO-H2O和三元体系DMSO-DMF-H2O在不同组成时的饱和蒸气压数据。用NRTL模型对二元数据进行了关联,用关联得到的二元模型参数计算了三元体系的饱和蒸气压数据,理论计算与实验值符合良好。利用NRTL模型预测了DMF占DMSO质量分数分别为1%、5%、10%时DMSO-DMF-H2O三元体系的常压汽液平衡数据。结果表明,少量DMF的加入对DMSO-H2O体系的汽液平衡影响较小,基本不影响DMSO-H2O的精馏分离效果,因此DMF有望作为一种良好的稳定剂用于DMSO-H2O精馏分离。

DMSO对悬浮培养的东北红豆杉细胞凋亡和紫杉醇合成的影响

研究了不同浓度的DMSO对悬浮培养的东北红豆杉 (Taxuscuspidata)细胞的增殖能力、细胞活性以及紫杉醇合成和释放等方面的影响 ,同时应用荧光指示剂双染法检测了细胞凋亡的发生情况。结果显示2 %的DMSO处理能显著降低细胞活性 ,抑制细胞的增殖能力 ,使细胞核内DNA含量减少 ,培养中、后期在荧光显微镜下可见部分细胞核出现典型的凋亡形态 ,同时伴有紫杉醇产量的明显增加 ;对照组及 1%以下浓度组未出现上述改变。结果表明一定浓度的DMSO能诱导细胞凋亡 。

玉米淀粉在DMSO/水体系中溶解性与精细结构变化

二甲亚砜(dimethyl sulfoxide,DMSO)是淀粉精细结构分析中溶解淀粉的关键试剂。以普通玉米淀粉为原料,研究其在DMSO/水体系中的溶解性与精细结构变化。结果表明,当溶解时间达到12h后,普通玉米淀粉在90%DMSO溶液中溶解性达到最大值97.15%;随着溶解时间的延长,溶解性无显著变化。扫描电镜(SEM)结果表明,90%的DMSO对淀粉颗粒结构破环最大,证明90%DMSO是淀粉的最佳溶剂。然而进一步通过高效液相体积排阻色谱联用系统(HPSEC)、阴离子色谱(HPAEC)等技术研究发现,淀粉溶于90%DMSO后,随着溶解时间的延长,其分子量和回旋半径逐渐下降,在溶解过程中淀粉分子发生了降解,主要降解部分为支链淀粉的B2、B3链,而B1链相对稳定。

钆在DMSO中的电化学研究

研究了二甲基亚砚（ＤＭＳＯ）中，钆在Ｐｔ和Ｃｕ电极上的电化学行为．结果表明，Ｇｄ（Ⅲ）在Ｐｔ和Ｃｕ电极上一步不可逆还原为Ｇｄ（０），在Ｃｕ电极上恒电位电解，可获得粘附性好的Ｇｄ均匀沉积膜，其中Ｇｄ含量（质量分数，％）可达９０．３．利用循环伏安法、电流－时间曲线、电位－时间曲线测定了Ｇｄ（Ⅲ）离子在３０１Ｋ下，Ｇｄ（ＣｌＯ４）３－ＬｉＣｌＯ４－ＤＭＳＯ溶液中的扩散系数和传递系数分别为２．０１×１０６ｃｍ２·ｓ－１和０．１７．

DMSO和NaSCN水溶液对PAN原液流变性能的影响

以二甲基亚砜(DMSO)和质量分数为51%的硫氰酸钠(Na SCN)水溶液为溶剂,分别配制质量分数为12%的PAN原液,对应为D原液、N原液,采用旋转流变仪对D原液、N原液的流变性能进行了研究。结果表明:N原液和D原液相比,N原液的黏度比较高,不存在零切黏度,结构比较复杂,稳定性比较差,拉伸强度和拉伸断裂形变比较高;N原液和D原液的线性粘弹区范围宽泛;N原液为粘性和弹性相当的流体,D原液为粘性大于弹性的流体。

DMSO对EC9706细胞端粒酶活性及生长的影响

目的 研究二甲基亚砜 (DMSO)对EC970 6细胞端粒酶活性及生长的影响。方法 用 1.3 %DMSO处理食管癌EC970 6细胞 ,TRAP -ELISA法检测细胞端粒酶活性的改变 ,流式细胞仪分析细胞周期的改变。结果 DMSO处理后的EC970 6细胞 ,端粒酶活性明显下降 ,且细胞周期明显改变 ,G1期细胞比率显著增高 ,S期细胞数显著降低。结论 DMSO可抑制EC970 6细胞端粒酶活性 ,使EC970 6细胞生长停滞于G1期 ,并诱导细胞凋亡。