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Phytonanotechnology
Published in Namrita Lall, Medicinal Plants for Cosmetics, Health and Diseases, 2022
Tafadzwa J. Chiome, Asha Srinivasan
With still a lot of work being done in cancer research, co-delivery has shown to be a viable option when it comes to improving the efficiency of cancer treatment by using nanocarriers for the dual loading of both phytochemicals and other anti-tumor agents. Such a delivery has shown to be efficient at: (i) improving drug solubility; (ii) increasing bioavailability; (iii) minimizing chances of drug resistance development; (iv) delaying cellular adaptation; (v) inducing simultaneous therapeutic effect; (vi) delivery of optimum dosage; and (vii) reduced systemic cytotoxicity. Some studies have been done on several phytochemicals in conjunction with anti-cancer drugs used as first line treatment and some of the studies are listed in Table 13.5.
A Treatise on the Role of Herpesvirus in Neurodegeneration
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Bernard W. Downs, Manashi Bagchi, Bruce S. Morrison, Jeffrey Galvin, Steve Kushner, Debasis Bagchi, Kenneth Blum
Autophagy, a unique but normal and natural mechanism for neuronal antiviral defense, has several beneficial functions, including (i) routine organelle and protein turnover, (ii) cellular adaptation to stress, and (iii) innate immunity against intracellular pathogens and viruses, as well as exerting a pivotal role in neuronal homeostasis in stress adaptation and viral infections. However, in neuronal cells, herpetic viral antagonism of autophagy will proceed toward neuronal dysfunction, degeneration, and death [8,9]. Orvedahl and Levine [10] explained how autophagy participates in boosting immunity and neuroprotection and further demonstrated how antagonism of autophagy participates in contributing to viral neurovirulence. As already indicated, autophagy provides a protective mechanistic role against alphaviruses and α-herpesviruses-induced encephalitis.
Critical Review of Evidence for Neonatal Cocaine Intoxication and Withdrawal
Published in Richard J. Konkol, George D. Olsen, Prenatal Cocaine Exposure, 2020
Delia A. Dempsey, Donna M. Ferriero, Sarah N. Jacobson
Tolerance and withdrawal are interrelated physiologic processes. Tolerance is a general phenomenon noted with many drugs and can involve various mechanisms. Tolerance includes the ability of those chronically exposed to a drug to tolerate doses that would be toxic in a naive user. Barbiturates, opiates, and ethanol are prime examples of drugs that induce tolerance. The mechanism of tolerance may be pharmacodynamic tolerance, where cellular adaptation to the drug takes place. Withdrawal represents the unopposed consequences of the cellular adaptation. The cells have adapted to the presence of the drug, but in the absence of the drug this response is maladaptive. Commonly, the signs and symptoms of withdrawal are the opposite of the pharmacologic effects of the drug. For example, withdrawal from sedative drugs usually produces excitation and agitation, while withdrawal from cocaine produces depression and somnolence.
Full-thickness dermal wound regeneration using hypoxia preconditioned blood-derived growth factors: A case series
Published in Organogenesis, 2023
Hadjipanayi Ektoras, Moog Philipp, Jiang Jun, Dornseifer Ulf, Machens Hans-Günther, Schilling Arndt F
Our bodies’ inherent ability to spontaneously heal small wounds quite efficiently, generates the question, why does the wound healing program stall when the wound surface area increases beyond a certain limit. While this still remains unclear, we had previously hypothesized that cellular adaptation to stress, specifically hypoxia (the key trigger for angiogenesis) may hamper cellular function.10,35,36,59 The spatial component of a wound is intrinsically interlinked with its temporal component, as wound healing normally progresses at a defined rate; wound healing in large wounds may progress at a slow pace relative to the spatial distance that needs to be covered (from the oxygenated free wound edge to the hypoxic wound center), which may result in cellular habituation to hypoxic stress, consequently altering the cell-driven angiogenic response. Without adequate vascular (i.e. nutrient/oxygen) supply, the regenerative cellular processes cannot operate optimally; therefore, impaired angiogenesis is likely the main cause for impaired cell differentiation, migration, proliferation and tissue remodeling. This could explain the ineffectiveness of passive wound healing treatments (e.g. dressings, vacuum-assisted closure, hydrating ointments etc.) to promote the repair of large wounds, despite the fact that they are beneficial for small wounds,60 since they lack the ability to provide bioactive support to the key angiogenic and contractile mechanisms.
Luteolin Induces Apoptosis and Autophagy in HCT116 Colon Cancer Cells via p53-Dependent Pathway
Published in Nutrition and Cancer, 2022
Ho Soo Yoo, Sae Bom Won, Young Hye Kwon
Autophagy is a pivotal component of the cellular adaptation in response to stress to maintain mammalian homeostasis by the degradation of cellular components to provide energy source and to eliminate the damaged cellular proteins and subcellular organelles. For these reasons, autophagy has been shown to protect against the development of several diseases, including neurodegenerative disease and cancer (Mizushima et al. 2008). Especially, dysregulation of autophagy is characterized as one of the key features associated with the development and progression of cancer. Therefore, a newer approach in cancer therapy that combines autophagy regulation with chemotherapeutic treatment may enhance cancer treatment. However, in a given context of neoplasia, including type, stage and extracellular milieu, the modulation of autophagy may either promote or suppress tumorigenesis (Mrakovcic and Frohlich 2018). Although several transcriptional targets of p53 can promote autophagy, the mechanisms of p53-dependent and -independent induction of autophagy are still incompletely understood.
The Subtle Role of Para-inflammation in Modulating the Progression of Dry Eye Disease
Published in Ocular Immunology and Inflammation, 2021
Maurizio Rolando, Stefano Barabino
One of the key pathways that regulates damage control, cellular adaptation to stress, and maintenance of homeostasis is autophagy, a sort of cleaning mechanism that allows cells to survive in response to degenerative, inflammatory, infectious, or neoplastic stressors.23, 24 The autophagic process is characterized by the formation of double-membraned vesicles, called autophagosomes, which sequester organelles, proteins, or portions of the cytoplasm, delivering them to the lysosomes, where they are degraded.25 Through this process, the cell does not only eliminate damaged or harmful cellular components that could act as stimuli for the activation of an inflammatory response but at the same time recycles these components to maintain nutrient and energy homeostasis.26,27