Treatment outcomes and patient satisfaction of a virtual partial hospital program: A mixed-method study.

OBJECTIVE: Despite a proliferation of virtual partial hospital programs (PHP) during the COVID-19 pandemic, there is a dearth of research on such programs. In the current study, we compared treatment outcomes and patient satisfaction between an in-person and a virtual PHP. Further, we examined patients' qualitative feedback about the virtual PHP. METHOD: Participants included 282 patients attending a virtual PHP during the COVID-19 pandemic and 470 patients attending an in-person PHP one year prior. Patients completed daily measures of symptom severity, and post-treatment measures of patient satisfaction and treatment outcomes. Patients in the virtual PHP provided feedback about virtual care. Quantitative data were analyzed using multilevel modeling, and qualitative data were analyzed using the principles of inductive analysis. RESULTS: Patients experienced a reduction in depression (b = -.28, p < .001) and anxiety symptoms (b = -.25, p < .001) over time and reported high satisfaction in both the in-person and virtual PHPs. There were no significant differences across programs. Virtual PHP patients identified unique advantages and disadvantages of virtual care. CONCLUSION: Our results suggest that virtual PHPs should be explored as an ongoing model of care that may help to systematically reduce barriers to accessing mental health services.

Mechanisms underlying somatostatin receptor 2 down-regulation of vascular endothelial growth factor expression in response to hypoxia in mouse retinal explants.

Hypoxia is a trigger of VEGF expression, the primary cause of retinal pathologies characterized by neovascularization. During hypoxia, transcription factors such as STAT3 and HIF-1 promote the increase in VEGF expression. Octreotide, a somatostatin receptor 2 (sst(2) )-preferring agonist, reduces retinal VEGF expression and neovascularization. To investigate the intracellular pathways linking sst(2) activation to the inhibition of hypoxia-induced VEGF up-regulation, we used pharmacological approaches and siRNA in mouse retinal explants cultured in normoxia or hypoxia. In hypoxic explants in which STAT3 or HIF-1 was inhibited, we observed the existence of reciprocal interactions between STAT3 and HIF-1, which synergistically induced VEGF expression. Octreotide prevented hypoxia-induced activation of STAT3 and HIF-1, and the downstream increase in VEGF expression, as evaluated in hypoxic explants treated with pharmacological inhibitors of STAT3 or HIF-1 and in normoxic explants in which pharmacological activators of STAT3 or HIF-1 were used to mimic a hypoxia-like response. The effect of octreotide on STAT3 activation is in part indirect, through the blockade of VEGFR-2 phosphorylation. The effect of octreotide on STAT3, HIF-1, VEGFR-2, and VEGF required Src homology region 2 domain-containing phosphatase 1 (SHP-1). In hypoxic extracts, octreotide induced SHP-1 phosphorylation and activation, and inhibiting SHP-1 abolished the octreotide effect on STAT3, HIF-1, VEGFR-2, and VEGF. The central role of SHP-1 in the modulation of STAT3 and HIF-1 was confirmed in normoxic explants in which pharmacologically activated SHP-1 prevented the effect of STAT3 or HIF-1 activation. Immunohistochemical studies showed that under hypoxia sst(2) and VEGF are expressed by retinal vessels, thus indicating a possible direct effect of octreotide on VEGF-containing endothelial cells. These data clarify the mechanism by which octreotide prevents hypoxia-induced VEGF up-regulation and support the effectiveness of octreotide in treatment of oxygen-induced retinopathies. These results may have implications in designing therapies targeting STAT3 and/or HIF-1 aimed at preventing retinal neovascularization.

Antiangiogenic effects of ß2 -adrenergic receptor blockade in a mouse model of oxygen-induced retinopathy.

Oxygen-induced retinopathy (OIR) is a model for human retinopathy of prematurity. In mice with OIR, beta-adrenergic receptor (ß-AR) blockade with propranolol has been shown to ameliorate different aspects of retinal dysfunction in response to hypoxia. In the present study, we used the OIR model to investigate the role of distinct ß-ARs on retinal proangiogenic factors, pathogenic neovascularization and electroretinographic responses. Our results demonstrate that ß(2) -AR blockade with ICI 118,551 decreases retinal levels of proangiogenic factors and reduces pathogenic neovascularization, whereas ß(1) - and ß(3) -AR antagonists do not. Determination of retinal protein kinase A activity is indicative of the fact that ß-AR blockers are indeed effective at the receptor level. In addition, the specificity of ICI 118,551 on retinal angiogenesis has been demonstrated by the finding that in mouse retinal explants, ß(2) -AR silencing prevents ICI 118,551 effects on hypoxia-induced vascular endothelial growth factor accumulation. In OIR mice, ICI 118,551 is effective in increasing electroretinographic responses suggesting that activation of ß(2) -ARs constitutes an important part of the retinal response to hypoxia. Lastly, immunohistochemical studies demonstrate that ß(2) -ARs are localized to several retinal cells, particularly to Müller cells suggesting the possibility that ß(2) -ARs play a role in regulating vascular endothelial growth factor production by these cells. The present results suggest that pathogenic angiogenesis, a key change in many hypoxic/ischemic vision-threatening retinal diseases, depends at least in part on ß(2) -AR activity and indicate that ß(2) -AR blockade can be effective against retinal angiogenesis.