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Future Developments in Human Thermography
Published in James Stewart Campbell, M. Nathaniel Mead, Human Medical Thermography, 2023
James Stewart Campbell, M. Nathaniel Mead
The transition from DCIS to an invasive breast cancer can be detected by thermography better than mammography. The activity of nitric oxide synthase (NOS) isoforms is significantly higher in DCIS than in normal surrounding tissues, and increased NOS activity may be associated with angiogenesis and the early development of invasive breast cancer and other cancers.28
Oxidative Stress and Inflammation
Published in Abhai Kumar, Debasis Bagchi, Antioxidants and Functional Foods for Neurodegenerative Disorders, 2021
Varsha Rana, Dey Parama, Sosmitha Girisa, Choudhary Harsha, Ajaikumar B. Kunnumakkara
Inflammation often leads to the activation of the inflammatory cells, which triggers the oxidant-generating enzymes such as inducible nitric oxide synthase (iNOS) and NOX. This results in the enhanced production of ROS and RNS (Murata et al., 2012). The ROS and RNS thus produced cause oxidative and nitrative DNA damage by inducing the formation of 8-oxo-7,8-dihydro-2′-deoxyguanosine (8-oxo-dG) and 8-nitroguanine, respectively. Additionally, iNOS generates NO in the inflammatory and epithelial cells. NO reacts with O2•−, which is produced by cytokines such as TNF-α as an inflammatory response, and results in the generation of peroxynitrite (ONOO−). This causes guanine nitration leading to the production of 8-nitroguanine, and subsequently causes nitrative DNA damage (Yermilov et al., 1995; Kawanishi et al., 2017).
The immune and lymphatic systems, infection and sepsis
Published in Peate Ian, Dutton Helen, Acute Nursing Care, 2020
Michelle Treacy, Caroline Smales, Helen Dutton
As sepsis progresses towards septic shock, endothelial damage increases nitric oxide synthase production; this is a potent vasodilator released from the endothelium. Now widespread vasodilatation and persistently leaking blood vessels lead to a gross maldistribution of the circulating volume. This, together with the intravascular micro-thrombi formation, causes a further imbalance between oxygen demand and oxygen supply to the tissues. As inflammation and increased permeability persist, a marked reduction in blood flow continues. This presents as hypotension with a narrow pulse pressure and exacerbates the pro-coagulant state. The body tries to regulate this process by releasing counter-inflammatory agents such as interleukins 4 and 10 and transforming growth factor-β (TGF β), but for some patients, the inflammation and ensuing endothelial changes become overwhelming (Nagalingam 2018). It is worth noting that the capillary refill, which was initially brisk, reduces as peripheral perfusion worsens. In the early phase of sepsis, as the heart tries to compensate for the persistently low systemic vascular resistance, the cardiac output may be high. Unfortunately, as sepsis progresses to septic shock, the myocardium is exposed to the circulation of substances such as myocardial depressant factor, which is synthesised by ischaemic pancreatic tissue, directly impairing myocardial contractility (Daniels and Nutbeam 2017).
Sepsis modulates aortic AT1 and P2Y6 receptors to produce vascular hyporeactivity in mice
Published in Journal of Receptors and Signal Transduction, 2023
T. Jagadeesh, Soumen Choudhury, Manju Gari, Vandana Singh, Amit Shukla, Satish K. Garg
Sepsis-induced hypo-reactivity is attributed to the induction of inducible-nitric oxide synthase (iNOS) activity and enhanced production of NO. Thus to assess the influence of iNOS on UDP and Ang-II-induced aortic contractions in sepsis, effects of both these agonists were recorded in the absence and presence of 1400 W, a selective inhibitor of iNOS, on endothelium-denuded arterial rings. As shown in Figure 8(C and D), the contractile response to UDP was not significantly altered in the presence of 1400 W (10 µM) in both the SO and CLP mice. Similarly, the contractile response to Ang-II was also not altered in the presence of 1400 W (10 µM) in SO mice (Figure 8(E)). However, contrary to the effect of UDP, the potency of Ang-II was significantly increased (8.62 ± 0.22 vs. 7.11 ± 0.23, n = 6) in the presence of 1400 W in septic mouse aorta as compared to its potency in the absence of 1400 W in CLP group (Figure 8(F)). However, there was no significant change in the maximal efficacy of Ang-II (0.04 ± 0.00 g, vs. 0.04 ± 0.00 g, n = 6).
Co Q10 improves vascular reactivity in male diabetic rats by enhancing insulin sensitivity and antioxidant effect
Published in Archives of Physiology and Biochemistry, 2023
Ghada E. Elgarawany, Ahmed Desoky Badawy, Suzan M. Hazzaa
Co Q10, Insulin, and combined treatment increased the vascular reactivity to NE and ACh when compared to diabetic untreated group. Insulin treatment stimulates alpha-adrenergic receptors in rat vascular smooth muscle cells (Kobayashi and Kamata 1999). Also, it induces nitric oxide production by stimulating nitric oxide synthase enzyme through its phosphorylation at serine and threonine residues (Perlstein et al.2012). It modulates the vascular reactivity inducing vasodilatation by activating NA+ K+ ATPase and NA+ K+ pump and decreasing Ca2+ influx via the voltage-gated channel (Davel et al.2000). On the other hand, Co-Q10 increases the vascular reactivity to NE and ACh via increasing insulin sensitivity, normalising blood glucose level and increasing the antioxidant levels with an improvement of endothelial function. Moreover, it increased the bioavailability of NO by decreasing the oxidised LDL (Tsai et al.2012). Oxidised LDL impairs endothelial nitric oxide synthase and NO-mediated vasodilatation (Wang et al.2011). Co-Q10 is a component of mitochondria and important in oxidative phosphorylation and ATP production. It has antioxidant activity directly through reaction with ROS or indirectly by the regeneration of ascorbate and tocopherol from the oxidised state (Tsai et al.2012). Co-Q10 deficiency is reported in various diseases including diabetes, heart disease, myopathy, and Parkinson’s diseases. So, Co-Q10 supplementation is considered a reason for its therapeutic effect (Gao et al.2012).
Cell penetrating peptides coupled to an endothelial nitric oxide synthase sequence alter endothelial permeability
Published in Tissue Barriers, 2022
Stephen R. Koch, Ryan J. Stark
The targeting and modification of intracellular processes that contribute to human pathophysiology remains an area ripe for discovery. This is no less true for diseases related to acute, systemic inflammation, such as sepsis, where targeted therapies have remained elusive.14 However, some of that difficulty can be attributed to the heterogenous and dynamic nature of sepsis, where therapies need to be given early and proactively to a cohort to impact outcomes. Within these cohorts are temporal alterations in nitric oxide producing enzymes that are critical for the regulation of vascular homeostasis. Nonspecific blockade of NO producing enzymes was demonstrated to be harmful in sepsis patients, clarifying their important role in the pathophysiology of human sepsis.6 Thus, providing a more specific or targeted approach to nitric oxide synthase pathways continues to be sought as a potential therapeutic avenue in sepsis.