miR-199a通过靶向ATP13A2抑制6-OHDA诱导的PC12细胞氧化应激

目的:探究miR-199a通过靶向调节ATP13A2对6-OHDA诱导的PC12细胞氧化应激的影响。方法:收集正常大鼠和帕金森(PD)模型大鼠脑组织,培养6-OHDA诱导的PC12细胞,利用Real-time PCR检测miR-199a和ATP13A2的表达,Western Blot检测ATP13A2表达。分别转染miR-199a类似物和miR-199a抑制剂,利用ELISA检测ROS、MDA、SOD和GSH-Px的表达。双荧光素酶报告基因检测miR-199a与ATP13A2的靶向关系。Western Blot法检测ATP13A2和JNK/c-Jun表达的影响。MTT法检测细胞增殖的影响。结果:PD脑组织和细胞中miR-199a表达显著降低,ATP13A2表达显著升高(P0.01)。过表达miR-199a可显著降低6-OHDA诱导的PC12细胞的ROS、MDA活性,升高SOD、GSH-Px活性(P0.01)。miR-199a过表达显著降低荧光素酶报告基因的荧光强度,而结合位点突变后荧光素酶活性不变(P0.01)。过表达miR-199a显著降低ATP13A2的表达并抑制JNK和c-Jun的磷酸化水平,茴香霉素则升高ATP13A2表达并激活JNK和c-Jun的磷酸化水平,过表达miR-199a且给予茴香霉素处理可使JNK和c-Jun的磷酸化水平恢复到6-OHDA-PC12组水平(P0.01)。过表达miR-199a抑制6-OHDA诱导的PC12细胞增殖,茴香霉素则促进其增殖,过表达miR-199a且给予茴香霉素处理可使细胞增殖率恢复到6-OHDA-PC12组水平(P0.01)。结论:miR-199a可通过靶向调节ATP13A2抑制6-OHDA诱导的PC12细胞氧化应激并抑制JNK/c-Jun活化。     

miR-449a通过靶向KLF4蛋白导致血管平滑肌细胞表型转化

目的探讨miR-449a对于血管平滑肌细胞表型转化、增殖和迁移的作用。方法首先构建携带miR-449a抑制剂、miR-449a mimic的质粒和携带KLF4 siRNA的病毒,并将其转染到血管平滑肌细胞当中,用即时荧光定量PCR检测miR-449a的量,用Western blot检测KLF4的表达量,并检测表型转化相关代表蛋白SM-MHC、α平滑肌肌动蛋白、骨桥蛋白。同时,用CCK-8和细胞划痕试验来评估细胞的增殖和迁移状况。用免疫荧光检测蛋白表达量及细胞结构变化。用荧光素酶报告基因实验来证实miR-449a与KLF4之间的关系。结果实验发现,miR-449a的下调可以增加KLF4的表达以此达到促进血管平滑肌细胞表型转化的作用,并增加其增殖和迁移能力。结论可以通过上调miR-449a降低KLF4的表达,从而抑制血管平滑肌细胞的表型转化及降低其增殖和迁移能力。     

七氟烷抑制人乳腺癌细胞系MCF-7增殖、迁移和侵袭

目的研究七氟烷对人乳腺癌细胞(MCF-7)增殖、迁移和侵袭的影响及其机制。方法用Western blot检测MCF-7细胞中高迁徙率族蛋白1 HMGB1的表达; miR-34a组(转染miR-34a mimics)、miR-con组(转染miR-con)、七氟烷处理+anti-miR-con组(转染anti-miR-con)及七氟烷处理+anti-miR-34a组(转染anti-miR-34a),均用脂质体法转染至MCF-7细胞; RT-qPCR检测细胞miR-34a表达; MTT法检测细胞增殖; Transwell小室法检测细胞迁移和侵袭;双荧光素酶报告基因实验检测细胞荧光活性。结果与对照组相比,1. 7%的七氟烷处理的细胞中miR-34a表达显著升高(P0. 05),HMGB1表达显著降低(P0. 05),且细胞增殖、迁移和侵袭均显著下调(P0. 05);过表达miR-34a可抑制MCF-7细胞增殖、迁移和侵袭,敲减miR-34a可降低七氟烷对MCF-7细胞增殖、迁移和侵袭的抑制作用。miR-34a可明显降低野生型HMGB1的细胞荧光活性,且负向调控HMGB1的表达。结论七氟烷可抑制人乳腺癌细胞增殖、迁移和侵袭。     

S100a7蛋白在体外培养人视网膜色素上皮细胞中的表达及功能

背景：S100a7蛋白在细胞增殖、血管形成等病理生理过程中发挥重要作用,但在视网膜色素上皮细胞中的作用少有报道。 目的：探讨S100a7蛋白在体外培养人视网膜色素上皮细胞中的表达及作用。 方法：体外培养ARPE-19细胞株,通过免疫荧光及Western blot技术,检测S100a7在ARPE-19细胞中的表达;不同稀释度(1∶1 000,1∶10 000,1∶100 000)S100a7蛋白抗体与ARPE-19细胞共培养,通过MTT技术检测S100a7蛋白在人视网膜色素上皮细胞增殖过程中的作用。 结果与结论：免疫荧光及Western blot技术证实该蛋白在ARPE-19细胞中表达;MTT实验结果显示,人视网膜色素上皮细胞加入S100a7抗体72 h后,各浓度处理组的吸光度值较对照组显著均降低(P < 0.05)。结果证实S100a7蛋白在人视网膜色素上皮细胞中的表达,并明显促进人视网膜色素上皮细胞增殖。     

抑制miR-23a-3p表达对人白血病细胞株HL-60侵袭和迁移的调节作用

目的探讨抑制miR-23a-3p表达对人白血病细胞株HL-60侵袭和迁移的影响及其分子机制。方法转染miR-23a inhibitor到HL-60细胞抑制miR-23a-3p的表达。HL-60细胞分为3组:HL-60组(阴性对照组)、scramble组(转染对照组)和miR-23a inhibitor组。qRT-PCR技术检测MMP-9和VEGF mRNA水平,Transwell实验检测细胞侵袭,划痕实验分析细胞迁移。Western blot法检测MMP-9和VEGF蛋白表达。结果转染scramble后HL-60细胞miR-23a-3p表达无明显变化。转染miR-23a inhibitor后HL-60细胞miR-23a-3p表达显著下降(P0.01)。scramble组与阴性对照组每个视野下的侵袭细胞数目差异无统计学意义。miR-23a inhibitor组每个视野下的侵袭细胞数目显著低于阴性对照组(P0.01)。scramble组与阴性对照组细胞迁移无明显差异。与阴性对照组相比,miR-23a inhibitor组细胞迁移显著降低(P0.01)。转染scramble不会影响MMP-9和VEGF的表达。miR-23a inhibitor组MMP-9和VEGF的mRNA水平显著低于阴性对照组(P0.01)。与阴性对照组相比,miR-23a inhibitor组MMP-9和VEGF的蛋白水平显著下降(P0.001)。结论抑制miR-23a-3p表达可减弱人白血病细胞株HL-60的侵袭和迁移。     

白花蛇舌草上调miR-485-5p抑制人膀胱癌细胞系KU-19-19增殖、迁移和侵袭

目的探讨白花蛇舌草对膀胱癌细胞系KU-19-19增殖、迁移和侵袭的影响和可能的分子机制。方法将KU-19-19细胞分为对照组、白花蛇舌草组、miR-NC组、miR-485-5p组、anti-miR-NC组、anti-miR-485-5p组、白花蛇舌草+anti-miR-NC组、白花蛇舌草+anti-miR-485-5p组、白花蛇舌草+anti-miR-485-5p+LY294002组。细胞计数试剂盒(CCK-8)、Transwell实验、实时荧光定量PCR(RT-qPCR)分别检测细胞增殖、迁移侵袭以及miR-485-5p的表达。蛋白质印迹(Western blot)检测磷脂酰肌醇-3-羟激酶(PI3K)和蛋白激酶B(AKT)的磷酸化水平。结果白花蛇舌草干预后KU-19-19细胞增殖率、迁移侵袭细胞数显著降低,miR-485-5p表达显著升高(P0.05);过表达miR-485-5p后,KU-19-19细胞增殖率、迁移侵袭细胞数显著降低(P0.05);抑制miR-485-5p表达后,KU-19-19细胞增殖率、迁移侵袭细胞数显著升高(P0.05)。抑制miR-485-5p可以逆转降低白花蛇舌草对KU-19-19细胞增殖、迁移和侵袭的抑制作用(P0.05);LY294002可以逆转降低抑制miR-485-5p对白花蛇舌草处理的KU-19-19细胞增殖、迁移和侵袭的促进作用(P0.05)。结论白花蛇舌草通过上调miR-485-5p可抑制膀胱癌细胞的增殖、迁移和侵袭,其机制可能与抑制PI3K/AKT信号通路有关。     

miR-451a通过靶向调节MEF2D抑制膀胱癌细胞的增殖、迁移和侵袭

目的研究miR-451a在膀胱癌中的表达及对膀胱癌发生发展的影响。方法通过实时定量PCR(real-time PCR)检测miR-451a在膀胱癌细胞系及组织标本中的表达。采用real-time PCR和Western blot检测MEF2D在膀胱癌组织及转染miR-451a mimics和inhibitor的T24细胞中的表达。双荧光素酶基因报告实验分析MEF2D是否为miR-451a直接的靶基因。通过MTT,Transwell迁移和侵袭实验检测T24细胞在转入miR-451a mimics和inhibitor后细胞增殖、迁移和侵袭能力的变化。结果 miR-451a在膀胱癌细胞及组织中的表达水平下调。miR-451a抑制了T24细胞的增殖、迁移和侵袭。双荧光素酶基因报告证实MEF2D为miR-451a的直接靶基因。miR-451a能够降低T24细胞MEF2DmRNA和蛋白表达水平。结论 miR-451a在膀胱癌中表达下调,通过靶向调节MDF2D起到了抑癌的作用,可能成为膀胱癌诊疗的潜在靶点。     

利多卡因通过LncRNA H19/miR-671-5p分子轴调控胃癌细胞增殖、迁移及侵袭北大核心CSCD

目的:探讨利多卡因对胃癌细胞增殖、迁移及侵袭的影响及其对LncRNA H19/miR-671-5p的调控机制。方法:体外培养胃癌细胞AGS,使用不同浓度的利多卡因处理细胞;MTT检测细胞增殖;Transwell小室实验检测细胞迁移及侵袭;qRT-PCR检测H19及miR-671-5p的表达量;双荧光素酶报告实验验证H19与miR-671-5p的靶向关系;将pcDNA-H19及其阴性对照pcDNA转染至AGS细胞,使用利多卡因处理细胞,采用上述方法检测细胞增殖、迁移及侵袭;Western blot检测增殖标记蛋白细胞增殖核抗原-67(Ki-67)、增殖细胞核抗原(PCNA)、上皮型钙黏蛋白(E-cadherin)、神经型钙黏蛋白(N-cadherin)的表达量。结果:与Con组相比,利多卡因不同剂量可明显降低细胞活力和Ki-67、PCNA、N-cadherin蛋白水平及H19的表达量(P<0.05),并可减少迁移及侵袭细胞数(P<0.05),提高E-cadherin蛋白水平及miR-671-5p的表达量(P<0.05);双荧光素酶报告实验证实H19可靶向结合miR-671-5p;H19过表达可明显逆转利多卡因对细胞增殖、迁移及侵袭的作用。结论:利多卡因可能通过抑制H19表达及促进miR-671-5p表达从而抑制胃癌细胞的增殖、迁移及侵袭。     

MiR-33a在胃癌组织中低表达并抑制HGC-27细胞增殖、迁移与侵袭

目的探讨miR-33a在胃癌患者中的表达,探讨miR-33a对胃癌HGC-27细胞增殖、侵袭和转移的影响。方法收集胃癌患者标本39例,同时收取相应的癌旁组织20例。通过荧光定量PCR方法检测各组织中miR-33a的表达水平。以脂质体为载体将miR-33a模拟物转染至HGC-27细胞,CCK-8方法检测细胞增殖能力变化,Transwell实验检测HGC-27细胞侵袭和迁移能力变化。结果 miR-33a在胃癌组织中的表达水平明显低于癌旁组织,过表达miR-33a能够显著抑制HGC-27细胞的增殖,显著抑制HGC-27细胞的侵袭和迁移能力。结论 miR-33a可能对胃癌有治疗作用。     

miR-34a 通过靶向SIRT1 对MPP+ 诱导的帕金森病模型细胞凋亡和氧化应激损伤的影响

目的:探讨miR-34a通过靶向SIRT1对MPP~+诱导的帕金森病模型细胞凋亡和氧化应激损伤的影响。方法:以MPP~+处理SH-SY5Y细胞建立帕金森病细胞模型,MTT法检测细胞存活率,RT-PCR检测细胞中miR-34a和SIRT1 mRNA的表达,Western blot检测SIRT1蛋白的表达。脂质体介导转染miR-34a模拟物和miR-34a抑制剂,RT-PCR和Western blot检测miR-34a对SIRT1 mRNA和蛋白表达的影响。采用荧光素酶实验检测miR-34a与SIRT1的靶向关系。将miR-34a抑制剂和SIRT1干扰序列转染至SH-SY5Y细胞后,采用流式细胞仪和LDH、SOD、MDA试剂盒分别检测miR-34a低表达靶向SIRT1对MPP~+诱导的SH-SY5Y细胞凋亡和氧化应激损伤的影响。结果:与对照组相比,500μmol/L、1 000μmol/L和2 000μmol/L MPP~+能够降低SH-SY5Y细胞的存活率、上调miR-34a和下调SIRT1表达(P0.05),且呈浓度依赖性。miR-34a模拟物可引起SIRT1 mRNA和蛋白表达降低,miR-34a抑制剂可引起SIRT1 mRNA和蛋白表达升高;荧光素酶实验证实SIRT1是miR-34a的靶基因。2 000μmol/L MPP~+可诱导SH-SY5Y细胞凋亡,细胞上清液中MDA含量和LDH活性显著升高,而SOD活性降低;转染miR-34a抑制剂成功下调miR-34a表达后可逆转MPP~+引起的上述变化,而转染SIRT1干扰序列成功下调SIRT1表达后可减弱miR-34a低表达引起的上述变化。结论:miR-34a低表达可通过靶向调控SIRT1抑制MPP~+诱导的帕金森病模型细胞凋亡和氧化应激损伤。     

An apparent KIR2DS2-negative KIR2DL2-positive genotype discloses the novel allele KIR2DS2*00104

KIR2DS2*00104 lacks a distinctive synonymous substitution of KIR2DS2 in nucleotide 418 that affects KIR genotyping.     

CaO-MgO-P_2O_5-SiO_2-CaF_2系统自硬性玻璃的研究

为研究钙离子、镁离子在体内环境中对自硬性玻璃结晶行为的影响,为自硬性生物活性玻璃的临床应用提供依据,本文设计了CaO-P2O5-SiO2-CaF2(Ca-glass)和CaO-MgO-P2O5-SiO2-CaF2(CaMg-glass)系统玻璃并使用模拟体液(simulated body flu id,SBF)进行了研究。首先采用磷酸氢二氨[(NH4)2HPO4]/[NH4H2PO4]硬化液与Ca-glass、CaMg-glass制成硬化体,然后使用X射线衍射(XRD)、扫描电镜(SEM)、失重、力学分析等方法,研究硬化体在SBF中的结晶性、降解性和力学性能。实验结果表明,玻璃粉末与磷酸铵缓冲溶液反应形成了磷酸铵钙[(NH4)2.Ca(HPO4)2.H2O]硬化体。硬化体经过SBF浸泡,Ca-glass系统硬化体中部分磷酸铵钙转化成羟基磷灰石,而CaMg-glass系统硬化体仍然为磷酸铵钙。Ca-glass与CaMg-glass硬化体在SBF中浸泡28天分别降解19.4%和31.3%,抗压强度分别为93.14MPa和64.52MPa。镁离子的歧化作用是导致Ca-glass、CaMg-glass硬化体结晶性能、降解性能以及力学性能差别的主要原因。     

K2O-B2O3-Al2O3-SiO2-MgO-F系统可切削生物微晶玻璃

目的 可切削微晶玻璃的制备温度高达1500 ℃以上,此特性严重制约其产业化发展.本文设计制备了K2O-B2O3-Al2O3-SiO2-MgO-F系统低温云母生物微晶玻璃,并探讨制备工艺对材料结构和性能的影响.方法 采用1300 ℃熔化工艺与600～750 ℃晶化热处理工艺制备微晶玻璃,通过X射线衍射分析方法研究微晶玻璃的晶相组成,利用扫描电子显微镜观察微晶玻璃的形貌,并通过显微硬度分析、高速砂轮切削实验考察微晶玻璃的可切削性能.结果 分别经过600 ℃、650 ℃、700 ℃、750 ℃晶化热处理2 h、4 h、8 h后,玻璃中均形成了主晶相为氟金云母的微晶玻璃,微晶玻璃的显微硬度为3～8 GPa.且随着晶化温度的升高,微晶玻璃层状结构逐渐明晰,但硬度不断下降,其可切削性持续提高.结论 低温下熔化K2O-B2O3-Al2O3-SiO2-MgO系统玻璃工艺降低了可切削微晶玻璃的制备温度和成本,利于产业化生产和推广应用.     

2-Perbromomethyl-2-oxazoline: a novel trifunctional initiator for the ring-opening polymerization of 2-methyl-2-oxazoline

Polymerization of 2-methyl-2-oxazoline was carried out using a trifunctional initiator, 2-perbromomethyl-2-oxazoline. The degree of polymerization (DP) of the resulting polymer was very close to the feed mole ratio of the monomer to initiator. The number-average molecular weight M?_n increased linearly with conversion, indicating the living nature of the propagating chain end. ¹H NMR and end-group analyses results are consistent with the proposal that the polymer possesses a star-shaped structure.     

Cross-Protection in Mice After Immunization with H2N2, H3N2, and Heq2Neq2 Influenza Virus Strains

Mice were vaccinated with the influenza viruses A/Japan/57 (H2N2), A/Hong Kong/68 (H3N2), and A/Equi/Miami/63 (Heq2Neq2) and the hemagglutinin and neuraminidase recombinants derived from these viruses. After infection with the parent viruses, protection was compared with serological findings. It was found that influenza vaccine protects not only against infection with a strain identical or closely related to the vaccine strain, but against heterologous strains as well. Vaccination with Hong Kong/68 and its neuraminidase recombinant resulted in a heterologous neuraminidase inhibition titer against Japan/57 and in a protection against infection with Japan/57. By contrast, after vaccination with Japan/57 and its neuraminidase recombinant, no relevant heterologous neuraminidase inhibition titer against Hong Kong/68 was observed, whereas a protection against infection with Hong Kong/68 did exist. A cross-protection between Hong Kong/68 and Miami/63, but no relationship in the hemagglutination or neuraminidase inhibition tests, was established in the preinfection sera. A one-way antigenic relationship between these viruses was confirmed by the rise of hemagglutinin or neuraminidase antibodies against Hong Kong/68 in the postinfection sera. No cross-protection or serological relationship existed between Miami/63 and Japan/57. Besides the hemagglutinin and neuraminidase, a third factor, the “mouse-protecting antigen,” was considered to contribute to the protection obtained. According to the protection observed, the mouse-protecting antigen of Hong Kong/68 virus is related to that of Japan/57 as well as Miami/63 virus. The mouse-protecting antigens of both Japan/57 and Miami/63 are related to that of Hong Kong/68.     

H2O2 enhances Ca2+ release from osteoblast internal stores

The physiological activity of osteoblasts is known to be closely related to increased intracellular Ca2+ activity ([Ca2+]i) in osteoblasts. The cellular regulation of [Ca2+]i in osteoblasts is mediated by Ca2+ movements associated with Ca2+ release from intracellular Ca2+ stores, and transmembrane Ca2+ influx via Na+-Ca2+ exchanger, and Ca2+ ATPase. Reactive oxygen species, such as H2O2, play an important role in the regulation of cellular functions, and act as signaling molecules or toxins in cells. In this study, we investigated the effects of H2O2 on cellular Ca2+ regulation in osteoblasts by measuring intracellular Ca2+ activities using cellular calcium imaging techniques. Osteoblasts were isolated from the femurs and tibias of neonatal rats, and cultured for 7 days. The cultured osteoblasts were loaded with a Ca2+-sensitive fluorescent dye, Fura-2, and fluorescence images were monitored using a cooled CCD camera, and subsequently analyzed using image analyzing software. The results obtained are as follows: (1) The osteoblasts with lower basal Ca2+ activities yielded a transient Ca2+ increase, a Ca2+ spike, while osteoblasts with higher basal Ca2+ activities showed a continuous increase in [Ca2+]i leading to cell death. (2) Ca2+ spikes, generated after removing Na+ from superfusing solutions, were blocked by H2O2 and this was followed by a sustained increase in Ca2+ activity. (3) ATP- induced Ca2+ spikes were inhibited by pretreating with H2O2 and this was followed by a continuous increase of [Ca2+]i. When cells were pretreated with the exogenous nitric oxide (NO) donor S-Nitroso-N-acetylpenicilance (SNAP, 50 microM), treatments of ATP (1 mM) induced a Ca2+ spike-like increase, but [Ca2+]i did not return to the basal level. (4) The expression of inositol- 1,4,5-triphosphate receptor (IP3R) was enhanced by H2O2. Our results suggest that H2O2 modulates intracellular Ca2+ activity in osteoblasts by increasing Ca2+ release from the intracellular Ca2+ stores.     

KIR2DL2/S2 and KIR2DS5 in alcoholic cirrhotic patients undergoing liver transplantation

IntroductionThe molecular mechanisms underlying alcoholic liver fibrosis and cirrhosis are not completely understood. Hepatic fibrosis involves the interplay of diverse cells and factors, including hepatic stellate cells (HSCs), Kupffer, NK cells, and T-lymphocyte subsets. Killer-cell immunoglobulin-like receptors (KIR) are membrane receptors involved in mediation between NK and activated HSCs, regulating NK cell function through their interaction with HLA-I molecules. The aim of this study was to analyse the genetic association between KIR genes and the susceptibility to or protection from alcoholic cirrhosis (AC) in a cohort of male AC patients undergoing liver transplantation (LT) with and without concomitant viral infections.Material and methodsKIR genotyping was performed in nuclear DNA extracted from 281 AC patients and compared with 319 male controls.ResultsSignificant differences between total AC patients and healthy controls were only found in the case of KIR2DL2 and KIR2DS5. KIR2DL2 was significantly underrepresented in non-viral AC patients (52.6% vs. 63.3%; p = 0.015), while patients heterozygous for KIR2DL2 were also underrepresented in the non-viral AC group compared with controls (p = 0.034). KIR2DS5 was overrepresented in this group compared with healthy controls (p = 0.002). All these observations were only evident in AC patients older than 54 years old.ConclusionsOur data suggest a contrary effect of KIR2DL2 and KIR2DS5 in AC patients older than 54 years, in whom the presence of KIR2DL2 appears to be protective against AC, whereas the presence of KIR2DS5 seems to promote the fibrotic process, particularly in patients with no associated viral infection.     

ExspiratorischepO2-undpCO2-Kurven bei Atmung von N2-, He- und Ar−O2-Gemischen

Zusammenfassung Zur Untersuchung der intrapulmonalen Gasmischung wurden an zehn Versuchspersonen die exspiratorischenpO₂- undpCO₂-Kurven fortlaufend und simultan massenspektrometrisch in Abhängigkeit vom Atemvolumen bei Atmung von Stickstoff-Sauerstoff-, Helium-Sauerstoff- und Argon-Sauerstoff-Gemischen registriert.Im Mischluftanteil wurden für den Abfall despO₂ von 75% auf 25% der Endamplitude im Mittel bei N₂–O₂-Atmung 81,6 ml, bei He–O₂-Atmung 66,1 ml und bei Ar–O₂-Atmung 71,9 ml benötigt. Die entsprechenden Zahlen für den Anstieg despCO₂ sind bei Atmung von N₂–O₂ 84,9 ml, von He–O₂ 68,5 ml und von Ar–O₂ 80.6 ml.DerpO₂ des Alveolarluftanteils sank während der letzten 300 ml Exspirationsvolumen bei Atmung des N₂–O₂-Gemisches im Mittel um 4,7 Torr, bei He–O₂ um 3,4 Torr und bei Ar–O₂ um 6,8 Torr. DerpCO₂ stieg gleichzeitig im Mittel bei Atmung des N₂–O₂-Gemisches um 2,8 Torr, bei He–O₂ um 2,1 Torr und bei Ar–O₂ um 3,7 Torr.Die Ursachen dieser Differenzen werden für den Mischluftanteil auf unterschiedliche Diffusions- und Strömungsbedingungen in den zentralen Lungenabschnitten zurückgeführt. Demgegenüber lassen sich die unterschiedlichen Partialdruckänderungen im Alveolarplateau durch Diffusion in den peripheren Lungenabschnitten und durch die Form der O₂ und CO₂-Bindungskurven erklären.Mit finanzieller Unterstützung der Europäischen Gemeinschaft für Kohle und Stahl durchgeführte Forschungsarbeit.     

13C NMR spectroscopy of 2-formamido-2-methylpropyl acrylate and poly(2-formamido-2-methylpropyl acrylate)

The synthesis and characterization of 2-formamido-2-methylpropyl acrylate (FMPA) is reported. ¹³C NMR spectra of FMPA in CDCl₃, CD₃OD, DMSO-d₆, DMF-d₇, and D₂O exhibit two pairs of lines for all seven carbon atoms at room temperature; the ratio of the two conformers varies moderately with solvent (21 : 79 to 41 : 59). The conformers are believed to involve strong internal hydrogen bonding which is not completely broken even by the addition of trifluoroacetic acid to CDCl₃ (1/1, v/v). However, the pairs of lines coalesce in turn as the temperature is raised to 120°C in DMSO-d₆. FMPA was polymerized at 35°C in DMF and CHCl₃, using a free radical initiator and the polymer was characterized by ¹³C NMR spectroscopy.