Abstract Information science and technology ( IT; Including computer and communication), Biotechnology (BT) and Nanotechnology (NT), are the three main technologies dominant in the 21st century. In nanotechnology, quantum size effects or surface effect (due to enhanced surface to volume ratio) can cause many new and interesting phenomena. In the literature there is also evidence that addition of small metal particles to semiconductors can enhance the optical properties of these semiconductor ¡Vnanoparticle hybrid systems. In this thesis, an electrochemical method is used to fabricate Au and ZnO nanoparticles. To characterize the samples we use various techniques like TEM (for the particle size and crystal structure), XRD (for structure, particle size analysis), Absorbance spectroscopy (for analyzing the optical properties of these systems), Photoluminescence (to study the mechanism of internal emission in the ZnO nanoparticles) On the theoretical part, some calculations based on the Drude model we computed and compared to the experimental absorbance spectrum of the samples.

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No description available.

Thesis (Ph. D.)--Ohio State University, 2008. / Title from first page of PDF file. Includes bibliographical references (p. 151-178).

Results are presented from NVT Monte Carlo simulations of a three-dimensional lattice model of a binary mixture of solvent and surfactant chains in which free self assembly is allowed. It is demonstrated that the model exhibits a critical micelle concentration together with cluster size distributions consistent with experiment and theory (minimum and maximum in the distribution within the micellar region). The weight average aggregation number, N[w], increases linearly with the square root of the concentration of micellised surfactant as predicted theoretically. The dilute solution excess chemical potential (beta[0n] --- beta[01]) is determined from the cluster size distribution. It is found to be a monotonically decreasing function of n with different functional forms for small and large clusters. A single analytical expression is found to describe the cluster size distribution and the X[1] versus X[a] curve on the concentration range from 0 to 5 vol. % . It is necessary to introduce an activity coefficient to accurately describe the behaviour of the model for amphiphile concentrations greater than 5 vol. % . The dependence of this expression on temperature and molecular interaction parameters is determined. Results are also presented for the simulation of longer chains. Following investigation of three of the models free parameters, regions of phase space in which 'spongy' structures and vesicles --- either spherical or tubular --- are successfully identified. A preliminary phase diagram is established by considering the variation in the cavity size distribution function. These results are discussed in relation with experimental data and existing phenomenological studies. An extension of the Configurational-bias Monte Carlo (CBMC) based on a self-avoiding walk using sites selected from subsets of sites known a priori available for the regrowth is also established. Its theoretical fondation is laid out together with a partial assessment of its efficiency relative to both the classic reptation and CBMC for the simulation of chains lying on a lattice of high coordination number. A methodology for the simulation of polyoxyethylene oxide (POE) surfactants using a cubic lattice of coordination number c = 26 is briefly discussed.

No description available.

The major phenolic lipids from natural and technical Cashew Nut-Shell Liquids were isolated by various techniques including precipitation, chemical purification, distillation, phase separation and chromatography. Cardanol, 3-pentadecyl phenol and cardol were polyethoxylated under base catalysed conditions and the products were characterised by both nmr and HPLC. Their surfactant properties were then analysed by surface tension measurements and their rates and extent of biodegradation were evaluated by means of a modified OECD screening test. The synthesis of the biosyntetic intermediate 2,4-dihydroxy-6-pentadecyl benzoic acid, by means of a Horner-Emmons modification to the Wittig reaction, is also reported. Some studies with cavitands are also reported, including the synthesis of some novel macrocycles and some sugar transport studies.

Kyoto University (京都大学) / 0048 / 新制・課程博士 / 博士(工学) / 甲第15392号 / 工博第3271号 / 新制||工||1492(附属図書館) / 27870 / 京都大学大学院工学研究科物質エネルギー化学専攻 / (主査)教授 垣内 隆, 教授 江口 浩一, 教授 安部 武志 / 学位規則第4条第1項該当

Bei bis zur Hälfte aller mit einer Frühgeburt vor 32 Gestationswochen endenden Schwangerschaften wird die Geburt durch eine Infektion auslöst. Die angestoßene Inflammationsreaktion kann bei der Schwangeren neben einer vorzeitigen Wehentätigkeit auch mit Fieber und dem Nachweis systemischer Entzündungszeichen einhergehen. Das ungeborene Kind ist zu einer eigenen Inflammationsreaktion fähig. Der histologische Nachweis einer Entzündungsreaktion in Chorion, Amnion und auch der Nabelschnur wird dabei als Nachweis der fetalen Amnioninfektion gewertet. Es wird angenommen, dass die pränatal einsetzende Inflammationsreaktion sowohl die frühpostnatale Lungenfunktion, als auch die Wirksamkeit exogen zugeführter Surfactantpräparationen zur Behandlung des Atemnotsyndroms reduziert. Vom 01.01.2007 bis zum 31.12.2010 wurden im Perinatalzentrum des Universitätsklinikums Würzburg insgesamt 243 Frühgeborene < 32+0 Schwangerschaftswochen (SSW) behandelt. In eine retrospektive Untersuchung konnten 83 Frühgeborene eingeschlossen werden, die maschinell beatmet worden waren und Surfactant erhalten hatten sowie eine histologische Untersuchung der Plazenta, Eihäute und Nabelschnur vorlag. Bei 14/83 Frühgeborenen lag eine histologische Chorioamnionitis vor. Diese bildeten die Chorioamnionits-Gruppe. Weitere 69 Frühgeborene ohne histologische Chorioamnionitis bildeten die Kontrollgruppe. Für die folgenden Charakteristika bestanden keine Gruppenunterschiede: Rate einer pränatalen Steroidgabe zur Lungenreifeinduktion; Tokolyse; Gestationsalter; Geschlecht; Anzahl von Mehrlingen; Geburtsgewicht. Allerdings fand sich in der Chorioamnionits-Gruppe kein hypotrophes Frühgeborenes (0/14), in der Kontrollgruppe jedoch 25/69 (p=0,008). In der Chorioamnionitis-Gruppe waren 8 von 14 Frühgeborene spontan geboren, in der Kontrollgruppe 12 von 69 (p=0,004). Ein vorzeitiger Blasensprung > 12 Stunden war der Geburt von 7/14 (50%) der Frühgeborenen in der Chorioamnionitis-Gruppe vorausgegangen (vs. 10/69 (14,5%) in der Kontrollgruppe; p=0,007). Es konnten keine signifikanten Unterschiede zwischen der Chorioamnionitis-Gruppe und der Kontrollgruppe für den radiologischen Schweregrad des RDS, der Anzahl wiederholter Surfactantsubstitutionen, der Beatmungsdauer, des zusätzlichen Sauerstoffbedarfs und der Beatmungsdrücke 12 und 24 Stunden nach Surfactantgabe gefunden werden. Es bestand lediglich ein Trend zu einer verzögerten und damit prolongierten Reduktion der Beatmungsdrücke in der Chorioamnionitis-Gruppe mit einem signifikant niedrigen Mittelwert der Beatmungsdrücke in der Chorioamnionitis-Gruppe 2 Stunden nach Surfactantgabe (22,8±6,3mbar vs. 19,2±4,3mbar; p=0,03). Ebenso bestanden keine signifikanten Unterschiede zwischen den Gruppen bzgl. Sterblichkeit, moderater und schwerer BPD, ROP und IVH. In der vorliegenden Untersuchung konnten keine signifikanten Unterschiede in der frühpostnatalen Schwere der Lungenerkrankung oder in der Rate chronischer Erkrankungen Frühgeborener < 32 SSW mit bzw. ohne histologische Chorioamnionits gefunden werden. / Up to the half of all preterm births < 32 weeks of gestational age are caused by an infection. The reaction to inflammation can cause preterm labor as well as fever or systemic signs of infection within the mother. The unborn child is able to an own inflammation reaction. The histologic findings of an infection within the chorion, the amnion or the umbilical cord are the proof of fetal infection of the amnion. It is believed, that the prenatal beginning of inflammation reaction reduces the early postnatal lungfunction as well as the effect of supplied surfactant for the treatment of respiratory distress syndrome. From 01.01.2007 until 31.12.2010 243 preterms < 32 weeks of gestation were treated at the neonatal intensive care unit at the university hospital in Würzburg. In this retrospective study 83 preterm infant were included, which were venilated, had received surfactant and had a histologic examination of their placenta, their membranes and their umbilical cord. 14 out of these 83 preterms showed histologic signs of chorioamnionitis. These preterms formed the choriomanionitis-group. The other 69 preterms without histologic signs of chorioamnionits formed the control group. Concerning the following characteristics there were no differences within the groups: rate of prenatal application of steroids to induce lung materation; tocolysis; gestational age; gender; number of twins; birthweight. Although there were no hypotrophic preterms within the chorioamnionits-group (0/14), but in the control group 25/69 (p=0,008). 8 out of 14 preterms within the chorioamnionitis group compared with 12 out of 69 preterms in the control group were delivered spontaneous (p=0,004). Delivery of 7 out of 14 preterms in the chorioamnionitis group followed rupture of the membranes > 12 hours before delivery (50%) compared to 10 out of 69 preterms in the control group ( 14,5%; p=0,007). There were no significant differences between the groups concerning the radiologic findings of respiratory distress syndrome, the number of surfactant applications, duration of ventilation, the need of additional oxygen or the ventilation pressures needed 12 and 24 hours after application of surfactant. There was just a trend of delayed and as a consequence prolonged reduction on needed ventilation pressure within the chorioamnionitis group with an significantly lower average of needed ventilation pressure 2 hours after application of surfactant (22,8+-6,3 mbar vs 19,2+-4,3 mbar; p=0,03). There were no significant differences within the groups concerning mortality, moderate or severe BPD, ROP or IVH.

Problématique : Le surfactant pulmonaire est une structure vitale essentielle à l’homéostasie pulmonaire. Étant composé majoritairement de phospholipides, il est particulièrement susceptible à l’oxydation puisqu’il est en constante interaction avec l’environnement extérieur. Par des mécanismes encore inconnus, les macrophages pulmonaires jouent un rôle majeur dans l’élimination du surfactant pulmonaire endommagé. Objectifs : 1) Caractériser la réponse transcriptionnelle et fonctionnelle des macrophages au surfactant pulmonaire sain et traité au peroxynitrite (ONOO⁻) et 2) investiguer le rôle de l’endocytose dans l’initiation de cette réponse. Méthodes : Des macrophages murins isolés par lavages bronchoalvéolaires ou différenciés de la moelle osseuse ont été exposés à du surfactant pulmonaire sain ou traité au ONOO⁻, avec ou sans Latrunculine A, un inhibiteur des mécanismes d’endocytose dépendant de l’actine. L’expression de gènes impliqués dans la capture (marco, msr1, cd36), l’accumulation intracellulaire (plin2) et l’export (abca1, abcg1, srb1) lipidique a été évaluée par qPCR, ainsi que les capacités fonctionnelles d’export lipidique. Résultats : L’addition de surfactant pulmonaire sain ou traité au ONOO⁻ augmente l’expression de marco, msr1, cd36 et plin2 et diminue l’expression d’abca1, abcg1 et scarb1 chez les macrophages. Toutefois, certaines différences transcriptionnelles ont été observées entre les macrophages pulmonaires primaires et ceux dérivés de moelle osseuse. Également, qu’il soit sain ou oxydé, le surfactant engendre une diminution des capacités d’efflux de cholestérol des macrophages différenciés. De plus, ces impacts transcriptionnels et fonctionnels ne semblent pas affectés par un traitement à la Latrunculine A. Conclusion : En présence de surfactant, et ce, indépendamment son niveau d’oxydation, les macrophages pulmonaires semblent favoriser les mécanismes de capture et d’accumulation lipidique. Ainsi, aux dépens de ces mécanismes priorisés, les deux espèces présentent conjointement une diminution à la fois transcriptionnelle et fonctionnelle des mécanismes d’export lipidique. / Problematic: Pulmonary surfactant is a vital structure essential to reduce the surface tension at the liquid-air interface. It is mainly composed of phospholipids and is susceptible to oxidation due to its close interaction with the external environment. Pulmonary macrophages play a major role in degrading damaged surfactant. However, the mechanisms used by pulmonary macrophages to detect and initiate its degradation are still unknown. Objectives: 1) To characterize the transcriptional and functional response of macrophages to native and peroxynitrite (ONOO⁻)-treated pulmonary surfactant and 2) to investigate the role of endocytosis in the initiation of this response. Methods: Primary mouse pulmonary macrophages isolated from bronchoalveolar lavages or differentiated from the bone marrow were exposed to native or ONOO⁻-treated pulmonary surfactant with or without endocytosis inhibitors (Latrunculin A). Expression of key genes implicated in lipid capture (msr1, marco, cd36), intracellular lipid accumulation (plin2), and lipid export (abca1, abcg1, scarb1) was assessed by quantitative PCR, as well as functional lipid export capacities. Results: The addition of native and ONOO⁻-treated pulmonary surfactant increased marco, msr1, cd36 and plin2 expression and decreased abca1, abcg1 and scarb1 expression in macrophages. However, some transcriptional differences were observed between primary and bone marrow macrophages. Also, both native and ONOO--treated pulmonary surfactant generated a decrease in differentiated macrophages cholesterol efflux capacities. Moreover, those transcriptional and functional impacts do not seem to be affected by Latrunculin A treatment. Conclusion: In the presence of pulmonary surfactant and this, independently its oxidation level, lung macrophages seem to promote lipid capture and storage mechanisms. Thus, depending on these prioritized mechanisms, the two species jointly showed a transcriptional and functional decrease in lipid export mechanisms.