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The intraoral scanner represents an important innovation in the world of dentistry, capable of transforming and digitizing conventional workflows and significantly improving communication with the patient, especially in pediatric age. The aim of this study is to investigate how digital dentistry, using the intraoral scanner, can interact in the communicative trinomial dentist–pediatric patient–parents and how this tool can be useful in communicating and understanding the received message. The value of the introduction of digital dentistry on communication schemes is evaluated by administering a questionnaire of 17 questions. A sample of 100 children aged between 6 and 12 years was studied. Of the sample of children/parents included in the study, 50 were re-examined 4 weeks after the first visit to re-administer the questionnaire. Internal consistency, assessed through Cronbach's alpha, was adequate, being alpha equal to 0.728. Test–retest reliability was assessed with Cohen's kappa index for dichotomous variables (percentage of agreement was >85.71%), and for the discrete variables it was assessed with the Intraclass Correlation Coefficient (ICC). The reliability was moderate (0.5 < ICC < 0.75) for Q4, Q9, Q11 and Q1; for the other answers, the reliability was poor (ICC < 0.5) and not statistically significant. The digital approach is confirmed not only as a powerful innovation from an engineering or clinical point of view, but also as a useful tool for a more effective communication in the approach to pediatric patients. [ABSTRACT FROM AUTHOR]

Currently 1.3 billion individuals globally engage in smoking, leading to significant morbidity and mortality, particularly among diabetic patients. There is urgent need for a better understanding of how smoking influences antidiabetic treatment efficacy. The review underscores the role of cigarette smoke, particularly polycyclic aromatic hydrocarbons (PAHs), in modulating the metabolic pathways of antidiabetic drugs, primarily through the induction of cytochrome P450 (CYP450) enzymes and uridine diphosphate (UDP)- glucuronosyltransferases (UGTs), thus impacting drug pharmacokinetics and therapeutic outcomes. Furthermore, the review addresses the relatively uncharted territory of how smoking cessation influences diabetes treatment, noting that cessation can lead to significant changes in drug metabolism, necessitating dosage adjustments. Special attention is given to the interaction between smoking cessation aids and antidiabetic medications, a critical area for patient safety and effective diabetes management. This scoping review aims to provide healthcare professionals with the knowledge to better support diabetic patients who smoke or are attempting to quit, ensuring tailored and effective treatment strategies. It also identifies gaps in current research, advocating for more studies to fill these voids, thereby enhancing patient care and treatment outcomes for this at-risk population. [ABSTRACT FROM AUTHOR]

Alzheimer's disease (AD) is the most common form of dementia worldwide, with a complex, poorly understood pathogenesis. Cerebral atrophy, amyloid-β (Aβ) plaques, and neurofibrillary tangles represent the main pathological hallmarks of the AD brain. Recently, neuroinflammation has been recognized as a prominent feature of the AD brain and substantial evidence suggests that the inflammatory response modulates disease progression. Additionally, dysregulation of calcium (Ca2+) homeostasis represents another early factor involved in the AD pathogenesis, as intracellular Ca2+ concentration is essential to ensure proper cellular and neuronal functions. Although growing evidence supports the involvement of Ca2+ in the mechanisms of neurodegeneration-related inflammatory processes, scant data are available on its contribution in microglia and astrocytes functioning, both in health and throughout the AD continuum. Nevertheless, AD-related aberrant Ca2+ signalling in astrocytes and microglia is crucially involved in the mechanisms underpinning neuroinflammatory processes that, in turn, impact neuronal Ca2+ homeostasis and brain function. In this light, we attempted to provide an overview of the current understanding of the interactions between the glia cells-mediated inflammatory responses and the molecular mechanisms involved in Ca2+ homeostasis dysregulation in AD. [ABSTRACT FROM AUTHOR]

Abstract This review will discuss some issues related to the risk/benefit profile of the use of dietary antioxidants. Thus, recent progress regarding the potential benefit of dietary antioxidants in the treatment of chronic diseases with a special focus on immune system and neurodegenerative disorders will be discussed here. It is well established that reactive oxygen species (ROS) play an important role in the etiology of numerous diseases, such as atherosclerosis, diabetes and cancer. Among the physiological defense system of the cell, the relevance of antioxidant molecules, such as glutathione and vitamins is quite well established. Recently, the interest of researchers has, for example, been conveyed on antioxidant enzyme systems, such as the heme oxygenase/biliverdin reductase system, which appears modulated by dietary antioxidant molecules, including polyphenols and beta-carotene. These systems possibly counteract oxidative damage very efficiently and finally modulate the activity of oxidative phenomena occurring, for instance, during pathophysiological processes. Although evidence shows that antioxidant treatment results in cytoprotection, the potential clinical benefit deriving from both nutritional and supplemental antioxidants is still under wide debate. In this line, the inappropriate assumption of some lipophylic vitamins has been associated with increased incidence of cancer rather than with beneficial effects.

Tumor necrosis factor‐related apoptosis‐inducing ligand (TRAIL), a cytokine belonging to the TNF superfamily, is regarded as a mediator of neurotoxicity. The constitutively expressed ion exchanger Na+/Ca2+ exchanger isoform‐3 (NCX3) has been shown to protect neurons from injury. Its expression is induced by nerve growth factor (NGF) through activation of its tyrosine kinase receptor trkA. The latter, in turn, activates downstream kinases, such as extracellular signal‐regulated kinase (ERK) and the survival‐related kinase protein kinase B (AKT). Here, we verified whether TRAIL could influence the expression of NCX3 via modulation of the NGF/trkA system. Differentiated human neuroblastoma SH‐SY5Y cells were incubated with TRAIL and, subsequently, the expression of the NCX3 protein was studied at different times by means of western blot analysis. Then, the expression of the phosphorylated forms of either trkA, ERK or AKT was analyzed at identical intervals. Western blot analysis revealed that the expression of NCX3 protein decreased in a time‐dependent fashion in SH‐SY5Y cells treated with TRAIL, to reach its minimum at 48 h. On the other hand, p‐trkA, p‐ERK, and p‐AKT expression was increased in cells treated with TRAIL after 6 and 16 h; then it declined to nearly undetectable levels after 48 h. Results indicate that the increase in TRAIL expression occurring during neuronal damage may be responsible of NCX3 down‐regulation and weakens its neuroprotective effects. The TRAIL system could thus represent a potential target for treatment of neuronal damage characterized by NCX3 function impairment. The potent neurotoxic cytokine tumor necrosis factor‐related apoptosis‐inducing ligand (TRAIL) modulates an array of intracellular pathways, including the cell survival‐related PI3K/protein kinase B (AKT) signaling. The neurotrophin nerve growth factor (NGF) induces up‐regulated expression of the neuroprotective Na+/Ca2+‐exchanger isoform‐3 (NCX3), via PI3K/AKT pathway. Increased expression of TRAIL occurring in neurodegeneration may represent a hurdle to beneficial effects of NGF on neurons, also via down‐regulation of NCX3 and inhibition of AKT phosphorylation. [ABSTRACT FROM AUTHOR]

Tumour necrosis factor-related apoptosis-inducing ligand ( TRAIL), a cytokine of the tumour necrosis factor superfamily, is a potent cell-apoptosis inducer, although its effects vary as a function of concentration. In fact, low concentrations of TRAIL are associated with non-apoptotic effects, such as cell proliferation. Here, the effects of TRAIL at different concentrations have been evaluated on mitogenesis and migration on human umbilical vein endothelial cells ( HUVEC) in vitro, as well as in the chick embryo chorioallantoic membrane ( CAM) angiogenesis model in vivo. At low concentrations, TRAIL promoted either mitogenesis or migration of HUVEC, evaluated using the wound healing method. Cleavage of caspase 8 was evaluated along with expression of the caspase 8-like molecule, cellular FLICE-inhibitory protein (long form) (c- FLIPL). Low concentrations of TRAIL failed to induce caspase 8 processing, whereas high concentrations induced apoptosis of HUVEC and activation of caspase 8. Moreover, TRAIL induced a significant angiogenic response in the CAM assay in vivo, comparable with that of vascular endothelial growth factor. These data suggest that the non-apoptotic effects of TRAIL include mitogenesis and increased mobility of endothelial cells, and eventually angiogenesis. In addition, the results demonstrate that the c- FLIPL level is also modulated by differences in TRAIL concentration, suggesting its involvement in the divergent effects of TRAIL. In conclusion, this study envisions a proangiogenic role of TRAIL, suggesting that TRAIL may represent a target for pharmacological manipulation. [ABSTRACT FROM AUTHOR]

Abstract: Kaposi''s sarcoma is a highly vascularized mesenchymal neoplasm arising with multiple lesions of the skin. Endogenous cannabinoids have been shown to inhibit proliferation of a wide spectrum of tumor cells. We studied the effects of cannabinoids on human Kaposi''s sarcoma cell proliferation in vitro. To do so, we first investigated the presence of the cannabinoid receptors CB1 and CB2 mRNAs in the human Kaposi''s sarcoma cell line KS-IMM by RT-PCR and, subsequently, the effects of the mixed CB1/CB2 agonist WIN-55,212-2 (WIN) on cell proliferation in vitro. WIN showed antimitogenic effects on Kaposi''s sarcoma cells. Western blot analysis of Kaposi''s sarcoma lysates suggested that WIN treatment induced activation of both caspase-3 and -6, as well as increased phosphorylation of the stress kinase p38 and JNK, along with transient phosphorylation of ERK1/2. To better characterize the involvement of each single CB receptor in cannabinoid-induced cell death, we incubated Kaposi''s sarcoma cells with different selective cannabinoid receptor agonists, respectively ACEA (CB1) and JWH-133 (CB2). None of the agonists was able to induce KS-IMM cell apoptosis. Moreover, we co-incubated Kaposi''s sarcoma cells with WIN-55,212-2 and either the CB1 receptor antagonist AM251, the CB2 receptor antagonist AM630, or a combination of both substances. The CB2 receptor antagonist AM630 was able to significantly increase survival of Kaposi''s sarcoma cells treated with WIN. In view of the antiproliferative effects of cannabinoids on KS-IMM cells, one could envision the cannabinoid system as a potential target for pharmacological treatment of Kaposi''s sarcoma. [Copyright &y& Elsevier]