65,066 research outputs found

    Chitin and lignin. Natural ingredients from waste materials to make innovative and healthy products for humans and plant

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    In a globalized world, plants are continually cut to obtain free land for intensive farming without remembering their important function in the planet ecosystem. They produce oxygen eliminating the carbon dioxide excess, contributing to reduce the pollution thus giving a great support to our health. According to the World Health Organization (WHO), air pollution -both outdoor and indoor- is nowadays "the biggest environmental risk to health carrying responsibility for about one in every nine deaths" (WHO, 2016). Outdoor pollution alone, in fact, kills around 3 million people each year. At this purpose however, it is necessary to remember that indoor emission of nanoparticles (NP) represent 50-80% of human exposure, calculated from 10.000 to 249.000 NP/mL air-while in polluted air NP are from ~10.000 to 50.000 NP/mL (Nohynek, 2011). Thus, there is a strict necessity "to consider air pollution as a global health priority in the sustainable development agenda" (WHO, 2016). Moreover, plants, multicellular organisms, as well as humans have evolved several mechanisms of defense and sensor systems to detect danger and prevent entry of most foreign material (Janeway et al, 2001). The sensors can direct and assist the host defenses by the use of specialized cells that ingest and digest foreign material. This protective non-specific method is called innate immune system, also connected with certain specific molecular patterns recognition associated with invading microbes or tissue damage (Nurnberger et al., 2004). In addition to innate immunity, vertebrates have evolved an adaptive immune system that relies on many antigen receptors, expressed by specialized immune cells. Unlike vertebrates, plants lack mobile defender cells and respond to infection by a two-branched immune system (Jones et al., 2006). The first branch recognizes and responds to all the common microbial molecules, while the second responds to pathogen virulence factors only. However, both plants and mammals have as first-line defense a barrier that, separating and shielding the interior of the body from the surrounding environment, represents the initial obstacle to be overcame from any pathogenic microorganisms. This barrier not only provides a physical separation, but releases also substances with antimicrobial properties. Moreover, when the first-line barrier has been breached, sensor systems are activated to give information to other components of the host defenses. Thus, while mammals activate, for example, the toll-like receptors capable to recognize families of compounds unique to microbes, plants release specialized compounds known as elicitors, signaling molecules able to induce their defense systems (Trouvelot et al., 2014). Examples of common ingredients, used from both plant and mammal as elicitors and defense-related compounds, are chitin and lignin. In this work, these materials will be briefly reviewed and results of chitin nanofibrils production and usage is reported. Finally, possible usage of combined chitin-lignin nanofibrils in commercial products will be pointed out

    The Immune System: the ultimate fractionated cyber-physical system

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    In this little vision paper we analyze the human immune system from a computer science point of view with the aim of understanding the architecture and features that allow robust, effective behavior to emerge from local sensing and actions. We then recall the notion of fractionated cyber-physical systems, and compare and contrast this to the immune system. We conclude with some challenges.Comment: In Proceedings Festschrift for Dave Schmidt, arXiv:1309.455

    G-protein-coupled receptors for free fatty acids: nutritional and therapeutic targets

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    It is becoming evident that nutrients and metabolic intermediates derived from such nutrients regulate cellular function by activating a number of cell-surface G-protein coupled receptors (GPCRs). Until now, members of the GPCR family have largely been considered as the molecular targets that communicate cellular signals initiated by hormones and neurotransmitters. Recently, based on tissue expression patterns of these receptors and the concept that they may elicit the production of a range of appetite- and hunger-regulating peptides, such nutrient sensing GPCRs are attracting considerable attention due to their potential to modulate satiety, improve glucose homeostasis and supress the production of various pro-inflammatory mediators. Despite the developing interests in these nutrients sensing GPCR both as sensors of nutritional status, and targets for limiting the development of metabolic diseases, major challenges remain to exploit their potential for therapeutic purposes. Mostly, this is due to limited characterisation and validation of these receptors because of paucity of selective and high-potency/affinity pharmacological agents to define the detailed function and regulation of these receptors. However, ongoing clinical trials of agonists of free fatty acid receptor 1 suggest that this receptor and other receptors for free fatty acids may provide a successful strategy for controlling hyperglycaemia and providing novel approaches to treat diabetes. Receptors responsive to free fatty acid have been of particular interest, and some aspects of these are considered herein

    The role of Microenvironment in tumorigenesis. Focus on dendritic cells in human papillomavirus E6, E7-transformed keratinocytes

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    The inception of tumor microenvironment (TME), a complex and dynamic system constituted by different types of cells engaged by tumor and extracellular matrix surrounding cancer cells, is a way for them to elude the immune surveillance. Dendritic cells (DCs), as a sentinel, are able to recognize alteration in the microenvironment and predispose the immune system response. The relationship between cancer and virus infection is well documented. High-risk Human Papillomavirus (HR-HPV) has a well-characterized transforming property and has been associated with squamous cell carcinoma of the ano-genital and oral tracts. Transforming ability of HR-HPVs is based on the function of E6 and E7 viral oncoproteins, which interact and inactivate p53 and pRb oncosuppressors, respectively. Recently, it was demonstrated that HPV oncoproteins are also able to affect a number of microRNAs (miRNAs) regulating the expression of genes involved in proliferative control. For these reasons DC-based vaccines targeting oncogenic E6 and E7 are ideal candidates to elicit strong immune responses. Here we summarize significant data about the analysis of TME in HPV-induced tumorigenesis. We also report original results produced by cytotoxic T lymphocyte (CTL) in vitro priming against E6 and E7 HPV16 antigens, performed using human monocyte-derived dendritic cells. Dendritic cells, maturated by the exposition to necrotic or apoptotic keratinocytes expressing both oncoproteins of HPV16, show different expression levels of specific maturation markers. Evidence indicating the ability of necrotic keratinocytes to alter the microRNA profile in DCs, macrophages (MΦ) and Langerhans cells (LCs) compared to prototypical stimuli as bacterial lipopolysaccharide was also provided. We can speculate that, based on transformed cells death pathway (i.e. apoptosis versus necrosis), virus-induced immune alterations might show different results in creating an immunotolerogenic microenvironment during the carcinogenesis process

    CAR-T cell. the long and winding road to solid tumors

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    Adoptive cell therapy of solid tumors with reprogrammed T cells can be considered the "next generation" of cancer hallmarks. CAR-T cells fail to be as effective as in liquid tumors for the inability to reach and survive in the microenvironment surrounding the neoplastic foci. The intricate net of cross-interactions occurring between tumor components, stromal and immune cells leads to an ineffective anergic status favoring the evasion from the host's defenses. Our goal is hereby to trace the road imposed by solid tumors to CAR-T cells, highlighting pitfalls and strategies to be developed and refined to possibly overcome these hurdles
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