Worse Sleep Quality Aggravates the Motor and Non-Motor Symptoms in Parkinson's Disease.

Backgrounds: Sleep disorders are the most common and disabling symptoms in patients with Parkinson's disease (PD). Understanding the associations between sleep characteristics and motor and non-motor symptoms (NMSs) in PD can provide evidence to guide therapeutic interventions and nursing strategies. We aimed to investigate the association between sleep characteristics and motor function and NMSs in PD using multiple approaches. Methods: A total of 328 participants were included, and all participants underwent Pittsburgh Sleep Quality Index (PSQI) evaluation and clinical assessments of PD symptoms. We conducted Spearman's correlation to evaluate the associations between sleep and PD symptoms, nonlinear regression to assess the relationships between sleep habits and PD, and mediated analyses to test the effects of NMSs on global PSQI and PD severity, quality of life, and motor symptoms. Results: Poor sleep was associated with more severe PD symptoms. In addition, the reflection point for bedtime was around 21:52, associated with motor symptoms, and insufficient and excessive total time spent in bed and nocturnal sleep duration were correlated with higher NMS burdens. The optimal points were 8-9.2 and 6.2-6.9 h, respectively. It was also discovered that NMSs played the mediating roles in global sleep with the quality of life, PD stages, and motor symptoms to a varying range of 6.8-95.4%. Conclusions: Sleep disorders have a significant effect on the burden of PD symptoms. The current findings provide new insights into the monitoring and management of sleep and PD and need to be further explored in the future studies.

Proliferation and differentiation of neural stem cells co-cultured with cerebral microvascular endothelial cells after oxygen-glucose deprivation / 华中科技大学学报（医学）（英德文版）

Various stem cells, including neural stem cells (NSCs), have been extensively studied in stroke models, but how to increase neuronal differentiation rate of NSCs remains unresolved, particularly in a damaged environment. The purpose of this study was to investigate the effects of cerebral microvascular endothelial cells (CMECs) on the neurogenesis of NSCs with or without oxygen-glucose deprivation (OGD). The NSCs acquired from primary culture were immunostained to prove cell purity. Survival and proliferation of NSCs were determined after the co-culture with CMECs for 7 days. After removing the CMECs, NSCs were randomly divided into two groups as follows: OGD and non-OGD groups. Both groups were maintained in differentiation culture for 4 days to evaluate the differentiation rate. Mouse embryo fibroblast (MEF) cells co-cultured with NSCs served as control group. NSCs co-cultured with CMECs had an increase in size (on the 7th day: 89.80±26.12 μm vs. 73.08±15.01 μm, P<0.001) (n=12) and number [on the 7th day: 6.33±5.61/high power objective (HP) vs. 2.23±1.61/HP, P<0.001] (n=12) as compared with those co-cultured with MEF cells. After further differentiation culture for 4 days, NSCs co-cultured with CMECs had an increase in neuronal differentiation rate in OGD and non-OGD groups, but not in the control group (15.16% and 16.07% vs. 8.81%; both P<0.001) (n=6). This study provided evidence that OGD could not alter the effects of CMECs in promoting the neuronal differentiation potential of NSCs. These findings may have important implications for the development of new cell therapies for cerebral vascular diseases.

Proliferation and differentiation of neural stem cells co-cultured with cerebral microvascular endothelial cells after oxygen-glucose deprivation / 华中科技大学学报（医学）（英德文版）

Various stem cells, including neural stem cells (NSCs), have been extensively studied in stroke models, but how to increase neuronal differentiation rate of NSCs remains unresolved, particularly in a damaged environment. The purpose of this study was to investigate the effects of cerebral microvascular endothelial cells (CMECs) on the neurogenesis of NSCs with or without oxygen-glucose deprivation (OGD). The NSCs acquired from primary culture were immunostained to prove cell purity. Survival and proliferation of NSCs were determined after the co-culture with CMECs for 7 days. After removing the CMECs, NSCs were randomly divided into two groups as follows: OGD and non-OGD groups. Both groups were maintained in differentiation culture for 4 days to evaluate the differentiation rate. Mouse embryo fibroblast (MEF) cells co-cultured with NSCs served as control group. NSCs co-cultured with CMECs had an increase in size (on the 7th day: 89.80±26.12 μm vs. 73.08±15.01 μm, P<0.001) (n=12) and number [on the 7th day: 6.33±5.61/high power objective (HP) vs. 2.23±1.61/HP, P<0.001] (n=12) as compared with those co-cultured with MEF cells. After further differentiation culture for 4 days, NSCs co-cultured with CMECs had an increase in neuronal differentiation rate in OGD and non-OGD groups, but not in the control group (15.16% and 16.07% vs. 8.81%; both P<0.001) (n=6). This study provided evidence that OGD could not alter the effects of CMECs in promoting the neuronal differentiation potential of NSCs. These findings may have important implications for the development of new cell therapies for cerebral vascular diseases.