Ana P.C. Almeida

Cellulose‐Based Biomimetics and Their Applications

Nature has been producing cellulose since long before man walked the surface of the earth. Millions of years of natural design and testing have resulted in cellulose-based structures that are an inspiration for the production of synthetic materials based on cellulose with properties that can mimic natural designs, functions, and properties. Here, five sections describe cellulose-based materials with characteristics that are inspired by gratings that exist on the petals of the plants, structurally colored materials, helical filaments produced by plants, water-responsive materials in plants, and environmental stimuli-responsive tissues found in insects and plants. The synthetic cellulose-based materials described herein are in the form of fibers and films. Fascinating multifunctional materials are prepared from cellulose-based liquid crystals and from composite cellulosic materials that combine functionality with structural performance. Future and recent applications are outlined.

Electron transfer and docking between cytochrome cd1 nitrite reductase and different redox partners - A comparative study.

Cytochrome cd1 nitrite reductases (cd1NiRs) catalyze the reduction of nitrite to nitric oxide in denitrifying bacteria, such as Marinobacter hydrocarbonoclasticus. Previous work demonstrated that the enzymatic activity depends on a structural pre-activation triggered by the entry of electrons through the electron transfer (ET) domain, which houses a heme c center. The catalytic activity of M. hydrocarbonoclasticus cd1NiR (Mhcd1NiR) was tested by mediated electrochemistry, using small ET proteins and chemical redox mediators. The rate of enzymatic reaction depends on the nature of the redox partner, with cytochrome (cyt) c552 providing the highest value. In situations where cyt c552 is replaced by either a biological (cyt c from horse heart) or a chemical mediator the catalytic response was only observed at very low scan rates, suggesting that the intermolecular ET rate is much slower. Molecular docking simulations with the 3D model structure of Mhcd1NiR and cyt c552 or cyt c showed that hydrophobic interactions favor the formation of complexes where the heme c domain of the enzyme is the principal docking site. However, only in the case of cyt c552 the preferential areas of contact and Fe-Fe distances between heme c groups of the redox partners allow establishing competent ET pathways. The coupling of the enzyme with chemical redox mediators was also found not to be energetically favorable. These results indicate that although low activity functional complexes can be formed between Mhcd1NiR and different types of redox mediators, efficient ET is only observed with the putative physiological electron donor cyt c552.

Elastomeric patterns probed by a nematic liquid crystal

GRAPHICAL ABSTRACT ABSTRACT Soft Janus elastomers have two surfaces with diverse characteristics. In this work, by tuning the chemical composition and the surface roughness we were able to vary the wettability of thin films (thickness of 100–200 μm) and spheres (diameters in the order of 200 μm to 2 mm) and evidence the multifunction of the opposite sides. We also describe a simple and inexpensive method to reveal the wrinkled-labyrinthine patterns that appear in the Janus particles by means of a nematic liquid crystal (LC). LC contact angle measurements associated with the swelling and anchoring characteristics of the surfaces were used to image the Janus particles opening new platforms for sensor applications from flexible free-standing LCs containers.

Hybrid polysaccharide-based systems for biomedical applications

Abstract Hybrid materials have been widely studied for structural applications. Polysaccharide-based fibers, especially cellulosic fibers, have been explored in the last two decades as substitutes of the traditional reinforcements made of glass or carbon fibers due to their mechanical properties. However, their biocompatibility, biodegradability, and chemistry have attracted the researchers and new developments in the field of smart and functional materials arise in diverse applications. This chapter will focus on the biomedical applications of polysaccharide-based smart and functional materials, namely those concerning biosensors and actuators, theranostic systems, and tissue-engineering applications. Special attention will be given to cellulose- and chitin/chitosan-based hybrid materials because these are the two most abundant polysaccharides and probably the most promising for the development of hybrid materials for biomedical applications. Biomimetic strategies for the development of smart and functional hybrid materials will also be highlighted.

Carbon monoxide targeting mitochondria in astrocytes: modulation of cell metabolism, redox response and cell death.

The endogenously produced gasotransmitter carbon monoxide (CO) has been studied as a factor involved in cytoprotection, homeostasis and anti-inflammation. Small amounts of reactive oxygen species (ROS) are described as signaling factors in CO’s biological mode of action. Mitochondria are the main source of ROS and are also key organelles in orchestrating cell function: metabolism, cell death control and redox signaling. Astrocytes are most abundant glial cells and essential for neuronal function, namely metabolic and physical support, expression of neurotransmitters and promotion of neuroprotection. In this work it is shown that CO prevents astrocytic cell death and improves cell metabolism by targeting mitochondria, and some of the underlying molecular mechanism are disclosed. CO directly targets non-synaptic mitochondria and inhibits their mitochondrial membrane permeabilization, by preventing mitochondrial swelling, depolarization and inner membrane permeabilization. Thus, CO limits the release of cytochrome c into the cytosol and the activation of apoptotic cascade in astrocytes. All these events are ROS-dependent and involve glutathionylation of adenine nucleotide translocator (ANT), whose activity is ATP/ADP transport through mitochondrial inner membrane. In addition, low amounts of exogenous CO increase ATP production by improving oxidative metabolism. Mitochondrial population and specific cytochrome c oxidase activity are higher upon CO treatment. The CO-induced metabolic improvement is dependent on Bcl-2 expression. Dysfunctional mitochondrial can be eliminated by mitophagy, which is a crucial process for maintaining their function and quality control. In astrocytes, CO promotes mitophagy at 1h of treatment, while following 24h mitochondrial population is back to basal levels, indicating that CO contributes to mitochondrial turnover. Furthermore, CO limits astrocytic cell death in an autophagic dependent manner.

Unravelling carbon monoxide protection in cerebral ischemia: from the organelle to the organism

Perinatal complications are a serious clinical problem, in particular hypoxic-ischemic (HI) episodes, caused by birth asphyxia or uterine and fetal blood flow interruption. HI corresponds to 23% of neonatal deaths, being one of the top 20 leading causes of disease burden. Preconditioning (PC) is a stimulation below the injury threshold that activates endogenous protective mechanisms to prevent damage. Low doses of carbon monoxide (CO) play a beneficial role through PC induction. Herein, CO cytoprotection was explored in distinct brain models. The used experimental models range from monoculture of astrocytes, co-cultures of neurons and astrocytes, to the whole organism with the rat model of perinatal ischemia. In primary cultures of astrocytic cells, CO not only impairs mitochondrial membrane permeabilization, by ANT glutathionylation, but also strengths mitochondrial oxidative metabolism, by modulating COX activity, increasing mitochondrial biogenesis and ATP amounts. Also, CO reinforces astrocytes-neurons communication towards neuronal survival. Purinergic molecules are the main mediators for this non-cell autonomous effect. Our results seem to indicate that the main pathway involved includes ATP release from astrocytes, its metabolization and A2A receptor binding to initiate protective mechanisms within the neurons. Rat pups were exposed to CO before hypoxia-ischemia induction (Vannucci model). 24h after HI the brains were collected for cell death and tissue protection assessment (histological and immunohistochemical analysis). It was found limited apoptosis in hippocampus following cerebral ischemia: lower cytochrome c release and caspase-3 activation yielding an increased Bcl-2 expression. Altogether, one can conclude that there is not just a unique pathway for the CO-induced endogenous protection, brain tolerance is the result of a complex cellular change in response to injury. Indeed, CO regulates cell death pathways and modulates cellular metabolism.