The effect of acceptance and commitment therapy on insomnia and sleep quality: A systematic review

Background Acceptance and Commitment Therapy (ACT), as a type of behavioral therapy, attempts to respond to changes in people’s performance and their relationship to events. ACT can affect sleep quality by providing techniques to enhance the flexibility of patients’ thoughts, yet maintaining mindfullness. Therefore, for the first time, a systematic review on the effects of ACT on sleep quality has been conducted. Methods This systematic review was performed to determine the effect of ACT on insomnia and sleep quality. To collect articles, the PubMed, Web of Science (WOS), Cochrane library, Embase, Scopus, Science Direct, ProQuest, Mag Iran, Irandoc, and Google Scholar databases were searched, without a lower time-limit, and until April 2020. Results Related articles were derived from 9 research repositories, with no lower time-limit and until April 2020. After assessing 1409 collected studies, 278 repetitive studies were excluded. Moreover, following the primary and secondary evaluations of the remaining articles, 1112 other studies were removed, and finally a total of 19 intervention studies were included in the systematic review process. Within the remaining articles, a sample of 1577 people had been assessed for insomnia and sleep quality. Conclusion The results of this study indicate that ACT has a significant effect on primary and comorbid insomnia and sleep quality, and therefore, it can be used as an appropriate treatment method to control and improve insomnia

Inhibition of vascular endothelial growth factor receptor reverses type 1 diabetes in nonobese diabetic mice. (112.17)

Abstract Small molecule receptor tyrosine kinase inhibitors (RTKI) represent a novel therapeutic avenue for the treatment of type 1 diabetes (T1D). These potential therapies target multiple kinases raising questions as to the precise target for intervention. In this investigation, we used a pharmacological approach to test whether vascular endothelial growth factor receptors (VEGF-R) participate in the regulation of disease pathogenesis in T1D in nonobese diabetic (NOD) mice. Treatment of new-onset diabetic NOD mice with PF-337210, an RTKI that inhibits the VEGF-R and platelet-derived growth factor receptors (PDGF-R), reversed diabetes. However, PDGF-R selective inhibitors did not, suggesting that VEGF-R are the principal targets mediating diabetes reversal. RTKI treatment of diabetic mice reduced insulitis, preserved islet mass and improved glucose tolerance, but had no effect on insulin resistance. Immunohistochemical studies suggested that the RTKI targeted VEGF-R expressed by the islet vasculature and not by leukocytes, suggesting that these drugs have a predominant effect on inflammatory processes that contribute to the pathogenesis of T1D rather than a direct effect on diabetogenic leukocytes. Collectively, the results show the inhibition of VEGF-R2 signaling can reverse diabetes by dampening inflammatory events that lead to islet dysfunction, and support the use of VEGF-R specific antagonists as novel therapeutics for the treatment of T1D.</jats:p

Inhibition of VEGF-R2 reverses type 1 diabetes in NOD mice by abrogating insulitis and restoring islet function. (P5181)

Abstract The dysregulation of receptor tyrosine kinases (RTKs) in multiple cell types during chronic inflammation is indicative of their pathogenic role in autoimmune diseases. Among the many RTKs, vascular endothelial growth factor receptor (VEGFR) stands out for its multiple effects on immunity, vascularization and cell migration. Herein, we examined whether VEGFR participated in the pathogenesis of type 1 diabetes (T1D) in non-obese diabetic (NOD) mice. We found that RTK inhibitors (RTKIs) and VEGF or VEGFR-2 antibodies reversed diabetes when administered at the onset of hyperglycemia. Increased VEGF expression promoted islet vascular remodeling in NOD mice, and inhibition of VEGFR activity with RTKIs abrogated the increase in islet vascularity, impairing T cell migration into the islet and improving glucose control. Metabolic studies confirmed that RTKIs worked by preserving islet function as treated mice had improved glucose tolerance without affecting insulin sensitivity. Finally, examination of human pancreata from patients with T1D revealed that VEGFR-2 was confined to the islet vascularity, which was increased in inflamed islets. Collectively, this work reveals an unappreciated role for VEGFR-2 signaling in the pathogenesis of T1D by controlling T cell accessibility to the pancreatic islets, and highlights a novel application of VEGFR-2 antagonists for the therapeutic treatment of T1D.</jats:p

Inhibition of VEGFR-2 reverses type 1 diabetes in NOD mice by abrogating insulitis and restoring islet function.

The dysregulation of receptor tyrosine kinases (RTKs) in multiple cell types during chronic inflammation is indicative of their pathogenic role in autoimmune diseases. Among the many RTKs, vascular endothelial growth factor receptor (VEGFR) stands out for its multiple effects on immunity, vascularization, and cell migration. Herein, we examined whether VEGFR participated in the pathogenesis of type 1 diabetes (T1D) in nonobese diabetic (NOD) mice. We found that RTK inhibitors (RTKIs) and VEGF or VEGFR-2 antibodies reversed diabetes when administered at the onset of hyperglycemia. Increased VEGF expression promoted islet vascular remodeling in NOD mice, and inhibition of VEGFR activity with RTKIs abrogated the increase in islet vascularity, impairing T-cell migration into the islet and improving glucose control. Metabolic studies confirmed that RTKIs worked by preserving islet function, as treated mice had improved glucose tolerance without affecting insulin sensitivity. Finally, examination of human pancreata from patients with T1D revealed that VEGFR-2 was confined to the islet vascularity, which was increased in inflamed islets. Collectively, this work reveals a previously unappreciated role for VEGFR-2 signaling in the pathogenesis of T1D by controlling T-cell accessibility to the pancreatic islets and highlights a novel application of VEGFR-2 antagonists for the therapeutic treatment of T1D