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Barbara Rothen-Rutishauser

Bio: Barbara Rothen-Rutishauser is an academic researcher from University of Fribourg. The author has contributed to research in topics: Nanoparticle & Medicine. The author has an hindex of 70, co-authored 339 publications receiving 17348 citations. Previous affiliations of Barbara Rothen-Rutishauser include University of Bern & Edinburgh Napier University.


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Journal ArticleDOI
TL;DR: Inhaled ultrafine titanium dioxide particles were found on the luminal side of airways and alveoli, in all major lung tissue compartments and cells, and within capillaries, while particle uptake in vitro did not occur by any of the expected endocytic processes, but rather by diffusion or adhesive interactions.
Abstract: High concentrations of airborne particles have been associated with increased pulmonary and cardiovascular mortality, with indications of a specific toxicologic role for ultrafine particles (UFPs; particles < 0.1 microm). Within hours after the respiratory system is exposed to UFPs, the UFPs may appear in many compartments of the body, including the liver, heart, and nervous system. To date, the mechanisms by which UFPs penetrate boundary membranes and the distribution of UFPs within tissue compartments of their primary and secondary target organs are largely unknown. We combined different experimental approaches to study the distribution of UFPs in lungs and their uptake by cells. In the in vivo experiments, rats inhaled an ultrafine titanium dioxide aerosol of 22 nm count median diameter. The intrapulmonary distribution of particles was analyzed 1 hr or 24 hr after the end of exposure, using energy-filtering transmission electron microscopy for elemental microanalysis of individual particles. In an in vitro study, we exposed pulmonary macrophages and red blood cells to fluorescent polystyrene microspheres (1, 0.2, and 0.078 microm) and assessed particle uptake by confocal laser scanning microscopy. Inhaled ultrafine titanium dioxide particles were found on the luminal side of airways and alveoli, in all major lung tissue compartments and cells, and within capillaries. Particle uptake in vitro into cells did not occur by any of the expected endocytic processes, but rather by diffusion or adhesive interactions. Particles within cells are not membrane bound and hence have direct access to intracellular proteins, organelles, and DNA, which may greatly enhance their toxic potential.

1,259 citations

Journal ArticleDOI
TL;DR: The factors that determine NP colloidal stability, the various efforts to stabilize NP in biological media, the methods to characterize NP colloid stability in situ, and a discussion regarding NP interactions with cells are examined.
Abstract: Nanomaterials are finding increasing use for biomedical applications such as imaging, diagnostics, and drug delivery. While it is well understood that nanoparticle (NP) physico-chemical properties can dictate biological responses and interactions, it has been difficult to outline a unifying framework to directly link NP properties to expected in vitro and in vivo outcomes. When introduced to complex biological media containing electrolytes, proteins, lipids, etc., nanoparticles (NPs) are subjected to a range of forces which determine their behavior in this environment. One aspect of NP behavior in biological systems that is often understated or overlooked is aggregation. NP aggregation will significantly alter in vitro behavior (dosimetry, NP uptake, cytotoxicity), as well as in vivo fate (pharmacokinetics, toxicity, biodistribution). Thus, understanding the factors driving NP colloidal stability and aggregation is paramount. Furthermore, studying biological interactions with NPs at the nanoscale level requires an interdisciplinary effort with a robust understanding of multiple characterization techniques. This review examines the factors that determine NP colloidal stability, the various efforts to stabilize NP in biological media, the methods to characterize NP colloidal stability in situ, and provides a discussion regarding NP interactions with cells.

733 citations

Journal ArticleDOI
TL;DR: The influence of particle size and surface chemistry are discussed, in order to understand the possible risks of nanoplastics for humans and provide recommendations for future studies.
Abstract: On account of environmental concerns, the fate and adverse effects of plastics have attracted considerable interest in the past few years. Recent studies have indicated the potential for fragmentation of plastic materials into nanoparticles, i.e., "nanoplastics," and their possible accumulation in the environment. Nanoparticles can show markedly different chemical and physical properties than their bulk material form. Therefore possible risks and hazards to the environment need to be considered and addressed. However, the fate and effect of nanoplastics in the (aquatic) environment has so far been little explored. In this review, we aim to provide an overview of the literature on this emerging topic, with an emphasis on the reported impacts of nanoplastics on human health, including the challenges involved in detecting plastics in a biological environment. We first discuss the possible sources of nanoplastics and their fates and effects in the environment and then describe the possible entry routes of these particles into the human body, as well as their uptake mechanisms at the cellular level. Since the potential risks of environmental nanoplastics to humans have not yet been extensively studied, we focus on studies demonstrating cell responses induced by polystyrene nanoparticles. In particular, the influence of particle size and surface chemistry are discussed, in order to understand the possible risks of nanoplastics for humans and provide recommendations for future studies.

611 citations

Journal ArticleDOI
TL;DR: Morphometric analysis of the CNS indicated unequivocally that the brain is a critical target for PM Exposure and implicated oxidative stress as a predisposing factor that links PM exposure and susceptibility to neurodegeneration.
Abstract: Particulate air pollution has been associated with respiratory and cardiovascular disease. Evidence for cardiovascular and neurodegenerative effects of ambient particles was reviewed as part of a workshop. The purpose of this critical update is to summarize the evidence presented for the mechanisms involved in the translocation of particles from the lung to other organs and to highlight the potential of particles to cause neurodegenerative effects. Fine and ultrafine particles, after deposition on the surfactant film at the air-liquid interface, are displaced by surface forces exerted on them by surfactant film and may then interact with primary target cells upon this displacement. Ultrafine and fine particles can then penetrate through the different tissue compartments of the lungs and eventually reach the capillaries and circulating cells or constituents, e.g. erythrocytes. These particles are then translocated by the circulation to other organs including the liver, the spleen, the kidneys, the heart and the brain, where they may be deposited. It remains to be shown by which mechanisms ultrafine particles penetrate through pulmonary tissue and enter capillaries. In addition to translocation of ultrafine particles through the tissue, fine and coarse particles may be phagocytized by macrophages and dendritic cells which may carry the particles to lymph nodes in the lung or to those closely associated with the lungs. There is the potential for neurodegenerative consequence of particle entry to the brain. Histological evidence of neurodegeneration has been reported in both canine and human brains exposed to high ambient PM levels, suggesting the potential for neurotoxic consequences of PM-CNS entry. PM mediated damage may be caused by the oxidative stress pathway. Thus, oxidative stress due to nutrition, age, genetics among others may increase the susceptibility for neurodegenerative diseases. The relationship between PM exposure and CNS degeneration can also be detected under controlled experimental conditions. Transgenic mice (Apo E -/-), known to have high base line levels of oxidative stress, were exposed by inhalation to well characterized, concentrated ambient air pollution. Morphometric analysis of the CNS indicated unequivocally that the brain is a critical target for PM exposure and implicated oxidative stress as a predisposing factor that links PM exposure and susceptibility to neurodegeneration. Together, these data present evidence for potential translocation of ambient particles on organs distant from the lung and the neurodegenerative consequences of exposure to air pollutants.

541 citations

Journal ArticleDOI
TL;DR: The following definitions for a nanoparticle (NP) and a nano-object will be used.
Abstract: Nanotechnology has become a key word of public interest, since people realized the social and economic power of nanotechnology development. Nanotechnology has already become part of our daily life, and it will have an as yet unknown technological impact because it concerns all aspects of human life from novel building materials to electronics, cosmetics, pharmaceutics, and medicine.1 In recent years, engineered nanoparticles started to become the most important components in nanotechnology. The InternationalOrganization for Standardization (ISO) has provided specific definitions in their recent document entitled “Nanotechnologies—Terminology and definitions for nanoobjects—Nanoparticle, nanofibre and nanoplate”. As the basis of this review, the following definitions for a nanoparticle (NP) and a nano-object will be used.

527 citations


Cited by
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[...]

08 Dec 2001-BMJ
TL;DR: There is, I think, something ethereal about i —the square root of minus one, which seems an odd beast at that time—an intruder hovering on the edge of reality.
Abstract: There is, I think, something ethereal about i —the square root of minus one. I remember first hearing about it at school. It seemed an odd beast at that time—an intruder hovering on the edge of reality. Usually familiarity dulls this sense of the bizarre, but in the case of i it was the reverse: over the years the sense of its surreal nature intensified. It seemed that it was impossible to write mathematics that described the real world in …

33,785 citations

28 Jul 2005
TL;DR: PfPMP1)与感染红细胞、树突状组胞以及胎盘的单个或多个受体作用,在黏附及免疫逃避中起关键的作�ly.
Abstract: 抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1(PfPMP1)与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用,在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员,通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

18,940 citations

Journal ArticleDOI
TL;DR: This review focuses on the characterization of EVs and on currently proposed mechanisms for their formation, targeting, and function.
Abstract: Cells release into the extracellular environment diverse types of membrane vesicles of endosomal and plasma membrane origin called exosomes and microvesicles, respectively. These extracellular vesicles (EVs) represent an important mode of intercellular communication by serving as vehicles for transfer between cells of membrane and cytosolic proteins, lipids, and RNA. Deficiencies in our knowledge of the molecular mechanisms for EV formation and lack of methods to interfere with the packaging of cargo or with vesicle release, however, still hamper identification of their physiological relevance in vivo. In this review, we focus on the characterization of EVs and on currently proposed mechanisms for their formation, targeting, and function.

6,141 citations