Ferrocenyl Dendrimers Based on Octasilsesquioxane Cores

Hydrosilylation reactions of two octasilsesquioxane dendritic cores containing terminal vinyl groups with bis­(ferrocenyl)­methylsilane (<b>1</b>) give dendrimers functionalized with 16 (<b>G1-Fc</b>_<b>16</b>) and 32 (<b>G2-Fc</b>_<b>32</b>) interacting ferrocenyl units. Characterization of the dendrimers by ¹H, ¹³C­{¹H}, and ²⁹Si­{¹H} NMR spectroscopy as well as mass spectrometry supports their assigned structures. The thermal behavior of dendrimers <b>G1-Fc</b>_<b>16</b> and <b>G2-Fc</b>_<b>32</b> was studied by TGA techniques. The redox activity of the ferrocenyl centers in <b>G1-Fc</b>_<b>16</b> and <b>G2-Fc</b>_<b>32</b> has been characterized by cyclic voltammetry and square wave voltammetry in dichloromethane containing [<i>n</i>-Bu₄N]­[PF₆] as electrolyte support. The solution voltammetric studies of the dendrimers <b>G1-Fc</b>_<b>16</b> and <b>G2-Fc</b>_<b>32</b> exhibit the pattern of communicating ferrocenyl sites with two distinct, separated oxidation waves. The dendrimers were also deposited on electrode surfaces and the electrodes investigated via CV, showing formation of electroactive films with promising results for the use of these materials in the development of biosensors

Synthesis and Electrochemical Anion-Sensing Properties of a Biferrocenyl-Functionalized Dendrimer

The synthesis and electrochemical anion-sensing properties of a diaminobutane poly­(propyleneimine) dendrimer functionalized with biferrocenyl units <b>2</b> are presented. The redox activity of the ferrocenyl centers in <b>2</b> has been characterized by cyclic voltammetry. Cyclic and square wave voltammetric investigations demonstrate that tetraferrocenyl compound <b>2</b> and the reference compound <b>1</b> show electrochemical anion-sensing action: they display a cathodic shift of the ferrocene–ferrocenium redox couple with dihydrogenphosphate and hydrogensulfate anions in solution and immobilized onto electrode surfaces

Using Heteroaryl-lithium Reagents as Hydroxycarbonyl Anion Equivalents in Conjugate Addition Reactions with (<i>S</i>,<i>S</i>)‑(+)-Pseudoephedrine as Chiral Auxiliary; Enantioselective Synthesis of 3‑Substituted Pyrrolidines

We have developed an efficient protocol for carrying out the stereocontrolled formal conjugate addition of hydroxycarbonyl anion equivalents to α,β-unsaturated carboxylic acid derivatives using (<i>S</i>,<i>S</i>)-(+)-pseudoephedrine as chiral auxiliary, making use of the synthetic equivalence between the heteroaryl moieties and the carboxylate group. This protocol has been applied as key step in the enantioselective synthesis of 3-substituted pyrrolidines in which, after removing the chiral auxiliary, the heteroaryl moiety is converted into a carboxylate group followed by reduction and double nucleophilic displacement. Alternatively, the access to the same type of heterocyclic scaffold but with opposite absolute configuration has also been accomplished by making use of the regio- and diastereoselective conjugate addition of organolithium reagents to α,β,γ,δ-unsaturated amides derived from the same chiral auxiliary followed by chiral auxiliary removal, ozonolysis, and reductive amination/intramolecular nucleophilic displacement sequence

Synthesis and Electrochemistry of ((Diferrocenylsilyl)propyl)- and ((Triferrocenylsilyl)propyl)triethoxysilanes

Triferrocenylsilane <b>2</b> was synthesized. Hydrosilylation reactions employing allyltriethoxysilane and diferrocenylmethylsilane (<b>1</b>) and triferrocenylsilane (<b>2</b>) yielded new ferrocenyltriethoxysilane compounds functionalized with two (<b>3</b>) and three (<b>4</b>) interacting ferrocenyl units, respectively. Characterization of <b>2</b> and the ethoxysilane derivatives <b>3</b> and <b>4</b> by elemental analysis, ¹H, ¹³C­{¹H}, and ²⁹Si­{¹H} NMR spectroscopy, and mass spectrometry supports their assigned structures. The crystal structure of <b>2</b> has been determined by a single-crystal X-ray diffraction study. The redox activity of the ferrocenyl centers in <b>2</b>–<b>4</b> has been characterized by cyclic voltammetry and square wave voltammetry in dichloromethane containing [<i>n</i>-Bu₄N]­[PF₆] or [<i>n</i>-Bu₄N]­[B­(C₆F₅)₄] as electrolyte support. Voltammetric studies of <b>2</b>–<b>4</b> in solution exhibit the pattern of communicating ferrocenyl sites with two or three distinct, separated oxidation waves. Platinum oxide surfaces are covalently modified by redox-active <b>3</b> and <b>4</b>

Coating Graphene Oxide with Lipid Bilayers Greatly Decreases Its Hemolytic Properties

Toxicity evaluation for the proper use of graphene oxide (GO) in biomedical applications involving intravenous injections is crucial, but the GO circulation time and blood interactions are largely unknown. It is thought that GO may cause physical disruption (hemolysis) of red blood cells. The aim of this work is to characterize the interaction of GO with model and cell membranes and use this knowledge to improve GO hemocompatibility. We have found that GO interacts with both neutral and negatively charged lipid membranes; binding is decreased beyond a certain concentration of negatively charged lipids and favored in high-salt buffers. After this binding occurs, some of the vesicles remain intact, while others are disrupted and spread over the GO surface. Neutral membrane vesicles tend to break down and extend over the GO, while vesicles with negatively charged membranes are mainly bound to the GO without disruption. GO also interacts with red blood cells and causes hemolysis; hemolysis is decreased when GO is previously coated with lipid membranes, particularly with pure phosphatidylcholine vesicles

H&E stained histopathological lung sections of mice 3 days post exposure.

<p>VC (A, B) and GO 162 μg/mouse (C, D, E, F). (A and B) No pathological changes. (C) Patchy appearance of acute pulmonary inflammation in areas with GO deposits (black arrows) in the parenchyma distal to the terminal and respiratory bronchioles, alveolar ducts, alveoli. (D) Free GO deposits (red arrow) and within alveolar cells (black arrows) in inflammatory area. Accumulation of granulocytes (green arrow). Hyperplastic type II cells (blue arrow). Congestion of vessels (CV). Alveolar granular exudate (AGE). (E) Patchy inflammation in peripheral section sites with GO deposits. Alveolar macrophage with GO in inflammatory lesion and in alveoli (black arrows), polymorphonuclear leukocytes (green arrow). Alveolar granular exudate (AGE). Hyperplastic type II cells (blue arrows). (F) Perivascular lymphoid accumulation (PVLA) with GO deposits.</p

H&E stained histopathological lung sections of mice 90 days post exposure.

<p>VC (A-C), GO 18 μg/mouse (D-F) or rGO 162 μg/mouse (G-I). (A-C) No pathological changes. (D-F) GO appeared as dark-brown pigments. Scattered prominent perivascular lymphoid accumulation (PVLA). Granuloma formation (GL) containing GO and macrophages with GO in alveoli (black arrows). Rare prominent perivascular lymphocytic accumulation (AGE). (G-I) Scarce accumulation of compact black rGO agglomerates (red arrows) and minimal tissue reactions.</p

DNA strand breaks.

<p>Level of DNA damage (Mean ± SEM) in BAL, lung and liver assessed with the comet assay (% DNA) 1, 3, 28 and 90 days post exposure to VC, GO, rGO or P90 (<i>n</i> = 7–8).</p

BAL fluid cell counts (x10³) (mean ±SEM) in mice at day 1, 3, 28 and 90 post exposure to VC (0.1% TW80), GO, rGO or Printex90 at doses 0, 18, 54 or 162 μg/mouse (<i>n</i> = 7–8).

<p>BAL fluid cell counts (x10³) (mean ±SEM) in mice at day 1, 3, 28 and 90 post exposure to VC (0.1% TW80), GO, rGO or Printex90 at doses 0, 18, 54 or 162 μg/mouse (<i>n</i> = 7–8).</p

Graphical presentation of the number of neutrophils in bronchoalveolar lavage (Mean ± SEM) from at day 1, 3, 28 and 90 following exposure to VC, GO, rGO or P90 (<i>n</i> = 7–8).

<p>*, ** and ***: Statistically significantly different from corresponding VC at level <i>p</i> < 0.05, <i>p</i> < 0.01, <i>p</i> < 0.001, respectively. ^#: GO statistically significantly different from corresponding rGO group at level <i>p</i> <0.001. For group GO 18 μg/mouse at day 1, the symbol is larger than the corresponding error bar. Therefore, the error bar is not visible (SEM is shown in <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0178355#pone.0178355.t002" target="_blank">Table 2</a>).</p