Association of residential greenness with geriatric depression among the elderly covered by long-term care insurance in Shanghai.

Residential greenness exposure has been linked to a number of physical and mental disorders. Nevertheless, evidence on the association between greenness and geriatric depression was limited and focused on developed countries. This study was aimed to investigate whether the relationship between residential greenness exposure and geriatric depression exists among the elderly with long-term care insurance (LTCI) in Shanghai, China. In 2018, a total of 1066 LTCI elderly from a cross-sectional survey completed a questionnaire in Shanghai. Residential greenness indicators, including normalized difference vegetation index (NDVI) and soil-adjusted vegetation index (SAVI), were calculated from the Landsat 8 imagery data in different buffers (100-m, 300-m, and 500-m). Mediation analysis by perceived social support was conducted to explore potential mechanisms underlying the associations. In the fully adjusted model, one IQR increase of NDVI and SAVI in the 300-m buffer size was associated with an 11.9% (PR: 0.881, 95% CI: 0.795, 0.977) and 14.7% (PR: 0.853, 95% CI: 0.766, 0.949) lower prevalence of geriatric depression, respectively. Stronger association was observed in the elderly with lower education level, living in non-central area, and lower family monthly income. Perceived social support significantly mediated 40.4% of the total effect for NDVI 300-m buffer and 40.3% for SAVI 300-m buffer to the greenness-depression association, respectively. Our results indicate the importance of residential greenness exposure to geriatric depression, especially for the elderly with lower education level, living in non-central area, and lower family monthly income. Perceived social support might mediate the association. Well-designed longitudinal studies are warranted to confirm our findings and investigate the underlying mechanisms.

Synergistic Effects of Aldehyde Dehydrogenase 2 Polymorphisms and Alcohol Consumption on Cognitive Impairment after Ischemic Stroke in Han Chinese.

Aldehyde dehydrogenase 2 (ALDH2) polymorphisms are related to both stroke risk and alcohol consumption. However, the influence of ALDH2 polymorphisms and alcohol consumption on cognitive impairment after ischemic stroke remains unknown, as do the possible mechanisms. We enrolled 180 Han Chinese ischemic stroke patients from four community health centers in Bengbu, China. Cognitive function was assessed using the Montreal Cognitive Assessment (MoCA), and two different MoCA cutoff scores were used to define cognitive impairment in ischemic stroke patients. The ALDH2 genotypes were determined using polymerase chain reaction and direct sequencing. To assess the associations of ALDH2 polymorphisms and alcohol consumption with cognitive impairment after ischemic stroke, we performed binary logistic regression analysis with odds ratios. We revealed that individuals with the ALDH2 wild-type genotype were more likely to have high MoCA scores than those with the mutant and heterozygous types (p = 0.034). In addition, using two MoCA cutoff scores, the percentage of moderate to excessive alcohol consumption in the cognitive impairment group was higher than that in the nonimpairment group (p = 0.001). The levels of 4-hydroxy-2-nonenal (p = 0.001) and swallowing function (p = 0.001) were also higher in the cognitive impairment group than in the nonimpairment group. Moreover, after adjusting for other potential risk factors, ALDH2 polymorphisms and alcohol consumption had a significant synergistic effect on cognitive impairment (p = 0.022). Specifically, the ALDH2∗2 mutant allele and higher alcohol consumption were associated with cognitive impairment and swallowing ability after ischemic stroke. Targeting ALDH2 may be a useful biomarker for cognitive rehabilitation following ischemic stroke.

Association of neighborhood greenness exposure with cardiovascular diseases and biomarkers.

AIM: Living in areas with neighborhood greenness may be associated with the incidence of cardiovascular diseases (CVDs). However, little evidence in this regard has emerged from developing countries. In the present study, we examined neighborhood greenness associated with CVDs and the lipid accumulation product (LAP) and pulse pressure (PP) in China. METHODS: We undertook our analysis using a community cross-sectional survey conducted in Longzihu District of Bengbu from July to August 2015. We measured triglyceride levels, waist circumference, and blood pressure. To assess exposure to neighborhood greenness, we used the average normalized difference vegetation index (NDVI) at 1,000-, 1,500-, and 2,000-m buffers in the participant community. We employed generalized mixed models to determine the association among neighborhood greenness, CVDs, LAP, and PP. We conducted stratified analysis by age, gender, income, and education. We assessed the potential mediating effects of road proximity and physical activity on greenness and CVDs, PP, and LAP. RESULTS: The highest tertiles of NDVI1500-m were steadily and significantly associated with lower odds of CVDs prevalence: the adjusted OR of such prevalence was 0.612 (95% CI, 0.462-0.811); higher NDVI was significantly associated with lower PP levels. The NDVI was strongly associated with CVDs prevalence among participants who were male and had high income. Ambient road proximity significantly mediated 9.7% of the estimated association between greenness and PP, there was no evidence of mediation effects for physical activity. CONCLUSIONS: Higher neighborhood greenness could have a beneficial effect on CVDs and biomarkers. There were higher associations between residential greenness and CVDs among male and higher-income individuals; road proximity partially mediated the observed association between greenness and PP.

Cross-sectional association of residential greenness exposure with activities of daily living disability among urban elderly in Shanghai.

AIM: Residential greenness exposure is associated with many health outcomes, including obesity, cardiovascular disease, and mental disorders. However, few studies have assessed the effects of greenness exposure on activities of daily living (ADL). This study evaluated the relationship between greenness and ADL among elderly residents with long-term care insurance (LTCI) in Shanghai, China. METHODS: We conducted a cross-sectional survey using stratified random sampling among elderly residents with LTCI in six districts of Shanghai in August 2018. We quantitatively assessed residential greenness using satellite-derived normalized difference vegetation index (NDVI) values with 250-, 500-, and 1000-m buffers around each participant's residential address. We calculated the walk score to assess neighborhood walkability. Physical function was assessed using basic ADL (BADL) and instrumental ADL (IADL). We performed binary logistic regression and restricted cubic splines with R software. RESULTS: The study participants were 1067 adults with a mean age of 82.40 years (standard deviation, 7.68 years). The mean NDVI value was 0.311. In the fully adjusted model, being in the highest-tertile NDVI500-m had a significant protective effect on BADL mild to none disability (odds ratio, 2.143; 95% confidence interval, 1.489-3.084) compared with participants in the lowest-tertile NDVI500-m. Restricted cubic spline showed a non-linearity association between NDVI values and BADL and IADL mild to none disability. CONCLUSIONS: Our results indicate the importance of residential greenness exposure to physical function-especially for BADL disability. Well-designed longitudinal studies are needed to confirm our findings and investigate the underlying mechanisms.

Collagen scaffold combined with human umbilical cord-mesenchymal stem cells transplantation for acute complete spinal cord injury.

Currently, there is no effective strategy to promote functional recovery after a spinal cord injury. Collagen scaffolds can not only provide support and guidance for axonal regeneration, but can also serve as a bridge for nerve regeneration at the injury site. They can additionally be used as carriers to retain mesenchymal stem cells at the injury site to enhance their effectiveness. Hence, we hypothesized that transplanting human umbilical cord-mesenchymal stem cells on collagen scaffolds would enhance healing following acute complete spinal cord injury. Here, we test this hypothesis through animal studies and a phase I clinical trial. (1) Animal experiments: Models of completely transected spinal cord injury were established in rats and canines by microsurgery. Mesenchymal stem cells derived from neonatal umbilical cord tissue were adsorbed onto collagen scaffolds and surgically implanted at the injury site in rats and canines; the animals were observed after 1 week-6 months. The transplantation resulted in increased motor scores, enhanced amplitude and shortened latency of the motor evoked potential, and reduced injury area as measured by magnetic resonance imaging. (2) Phase I clinical trial: Forty patients with acute complete cervical injuries were enrolled at the Characteristic Medical Center of Chinese People's Armed Police Force and divided into two groups. The treatment group (n = 20) received collagen scaffolds loaded with mesenchymal stem cells derived from neonatal umbilical cord tissues; the control group (n = 20) did not receive the stem-cell loaded collagen implant. All patients were followed for 12 months. In the treatment group, the American Spinal Injury Association scores and activities of daily life scores were increased, bowel and urinary functions were recovered, and residual urine volume was reduced compared with the pre-treatment baseline. Furthermore, magnetic resonance imaging showed that new nerve fiber connections were formed, and diffusion tensor imaging showed that electrophysiological activity was recovered after the treatment. No serious complication was observed during follow-up. In contrast, the neurological functions of the patients in the control group were not improved over the follow-up period. The above data preliminarily demonstrate that the transplantation of human umbilical cord-mesenchymal stem cells on a collagen scaffold can promote the recovery of neurological function after acute spinal cord injury. In the future, these results need to be confirmed in a multicenter, randomized controlled clinical trial with a larger sample size. The clinical trial was approved by the Ethics Committee of the Characteristic Medical Center of Chinese People's Armed Police Force on February 3, 2016 (approval No. PJHEC-2016-A8). All animal experiments were approved by the Ethics Committee of the Characteristic Medical Center of Chinese People's Armed Police Force on May 20, 2015 (approval No. PJHEC-2015-D5).

Hypoxia inhibits pulmonary artery endothelial cell apoptosis via the e-selectin/biliverdin reductase pathway.

Hypoxia-induced inhibition of apoptosis in pulmonary artery endothelial cells (PAECs) has an important role in pulmonary arterial remodeling leading to aggravated hypoxic pulmonary arterial hypertension. However, the mechanisms involved in the hypoxia-induced inhibition of PAEC apoptosis have not been elucidated. e-selectin and biliverdin reductase (BVR) have been reported to contribute to the cascade of apoptosis in several cell lines but not in PAECs. In the present study, we show that the expression of e-selectin and BVR was both up-regulated by hypoxia in PAECs. Moreover, hypoxia attenuated the decreased cell survival and apoptotic protein expression, and increased DNA fragmentation induced by serum deprivation in the PAECs, which was mediated by the e-selectin/BVR pathway. In addition, by examining the mitochondrial membrane potential and mitochondrial membrane proteins (Bcl-2 and BAX), we show that the mitochondrial-dependent apoptosis pathway was necessary for the e-selectin/BVR pathway inducing the anti-apoptotic effect of hypoxia in PAECs. Taken all together, our data show that the e-selectin/BVR pathway participates in the inhibitory process of hypoxia in PAEC apoptosis which is mediated by the mitochondrial-dependent apoptosis pathway.

15-PGDH/15-KETE plays a role in hypoxia-induced pulmonary vascular remodeling through ERK1/2-dependent PAR-2 pathway.

We have established that 15-hydroxyeicosatetraenoic acid is an important factor in regulation of pulmonary vascular remodeling (PVR) associated with hypoxia-induced pulmonary hypertension (PH), which is further metabolized by 15-hydroxyprostaglandin dehydrogenase (15-PGDH) to form 15-ketoeicosatetraenoic acid (15-KETE). However, the role of 15-PGDH and 15-KETE on PH has not been identified. The purpose of this study was to investigate whether 15-PGDH/15-KETE pathway regulates hypoxia-induced PVR in PH and to characterize the underlying mechanisms. To accomplish this, Immunohistochemistry, Ultra Performance Liquid Chromatography, Western blot, bromodeoxyuridine incorporation and cell cycle analysis were preformed. Our results showed that the levels of 15-PGDH expression and endogenous 15-KETE were drastically elevated in the lungs of humans with PH and hypoxic PH rats. Hypoxia stimulated pulmonary arterial smooth muscle cell (PASMC) proliferation, which seemed to be due to the increased 15-PGDH/15-KETE. 15-PGDH/15-KETE pathway was also capable of stimulating the cell cycle progression and promoting the cell cycle-related protein expression. Furthermore, 15-KETE-promoted cell cycle progression and proliferation in PASMCs depended on protease-activated receptor 2 (PAR-2). ERK1/2 signaling was likely required for 15-PGDH/15-KETE-induced PAR-2 expression under hypoxia. Our study indicates that 15-PGDH/15-KETE stimulates the cell cycle progression and proliferation of PASMCs involving ERK1/2-mediated PAR-2 expression, and contributes to hypoxia-induced PVR.