A comprehensive analysis of the crop effect on the urban-rural differences in land surface phenology.

The response of land surface phenology (LSP) to the urban heat island effect (UHI) is a useful biological indicator for understanding how vegetated ecosystems will be affected by future climate warming. However, vegetation cover in rural areas is often dominated by cultivated land, whose phenological timing is considerably influenced by agricultural managements (e.g., timing of sowing and harvesting), leading to biased conclusions derived from the urban-rural LSP differences. To demonstrate this problem, we investigated the crop influence on the phenological response to a warmer environment resulting from the UHI effect. We partitioned cities in the United States into cultivated and non-cultivated categories according to the proportion of crops in rural areas. We then built continuous buffer zones starting from the urban boundary to explore the urban-rural LSP differences considering the UHI effect on them. The results suggest crop inclusion is likely to lead to >14 days of urban-rural differences at both the start of the season (SOS) and the end of the season (EOS) between cultivated and non-cultivated cities. The temperature sensitivity (ST) of SOS is overestimated by approximately 2.7 days/°C, whereas the EOS is underestimated by 3.6 days/°C. Removing crop-dominated pixels (i.e., above 50 %) can minimize the influence of crop planting/harvesting on LSP and derive reliable results. We, therefore, suggest explicit consideration of crop impacts in future studies of phenological differences between urban and rural areas and the UHI effect on LSP in urban domains, as presented by this comprehensive study.

HACE1 expression in heart failure patients might promote mitochondrial oxidative stress and ferroptosis by targeting NRF2.

BACKGROUND: Heart failure is a prevalent and life-threatening medical condition characterized by abnormal atrial electrical activity, contributing to a higher risk of ischemic stroke. Atrial remodelling, driven by oxidative stress and structural changes, plays a central role in heart failure progression. Recent studies suggest that HACE1, a regulatory gene, may be involved in cardiac protection against heart failure. METHODS: Clinical data analysis involved heart failure patients, while an animal model utilized C57BL/6J mice. RT-PCR, microarray analysis, histological examination, ELISA, and Western blot assays were employed to assess gene and protein expression, oxidative stress, and cardiac function. Cell transfection and culture of mouse atrial fibroblasts were performed for in-vitro experiments. RESULTS: HACE1 expression was reduced in heart failure patients and correlated negatively with collagen levels. In mouse models, HACE1 up-regulation reduced oxidative stress, mitigated fibrosis, and improved cardiac function. Conversely, HACE1 knockdown exacerbated oxidative stress, fibrosis, and cardiac dysfunction. HACE1 also protected against ferroptosis and mitochondrial damage. NRF2, a transcription factor implicated in oxidative stress, was identified as a target of HACE1, with HACE1 promoting NRF2 activity through ubiquitination. CONCLUSIONS: HACE1 emerges as a potential therapeutic target and diagnostic marker for heart failure. It regulates oxidative stress, mitigates cardiac fibrosis, and protects against ferroptosis and mitochondrial damage. The study reveals that HACE1 achieves these effects, at least in part, through NRF2 activation via ubiquitination, offering insights into novel mechanisms for heart failure pathogenesis and potential interventions.

Effects of Nursing Care for the Treatment of Patients with Bladder Cancer: A Systematic Review and Meta-analysis.

Purpose: In this study, a systematic review and meta-analysis were used to examine the effectiveness of nursing care in the treatment of bladder cancer patients. The platforms of PubMed, Embase, Cochrane Library, and Web of Science were used to conduct a thorough literature search. Methods: The searching approach was used to find the fundamental characteristics of 5 studies. Sample size ranged from 52 to 131,852, and total sample size was 151,166. The study was looked up in PubMed, Embase, and Web of Science, with the most recent search being done in July 2022. Utilizing a standardized form, two independent reviewers gathered pertinent information from research that qualified as literature (17). Review Manager 5.3 used the data to examine the literature. Statistics were deemed significant at p < 0.05. Results: We discovered that more bladder cancer patients with T1+T2 tumor stages were receiving nursing care than those with T1+T2 tumor stages were receiving control care (mean difference =1.27, 95% CI: 1.20-1.35, p < 0.00001). The proportion of bladder cancer patients with T3+T4 tumor stage in the nursing care group was lower than the proportion of patients with T3+T4 tumor stage in the control group (mean difference = 1.07; 95% CI: 1.01-1.14; p < 0.00001). The difference between the number of bladder cancer patients receiving radiotherapy in the nursing care group and the control group was not statistically significant (mean difference = 1.07, 95% confidence interval [CI]: 0.99-1.16, p = 0.11). There were fewer patients with bladder cancer receiving chemotherapy in the nursing care group than that in the control group (mean difference = -0.02, 95% CI: -0.0-0.02, p < 0.00001). The incidence rate of patients with bladder cancer with major complications in nursing care group was lower than that of patients with bladder cancer with major complications in control group (mean difference = 0.41 95% CI: 0.18-0.93, p = 0.03). When compared to patients with bladder cancer who had serious complications in the control group, the hospital death rate for nursing care patients had a greater incidence of bladder cancer patients (mean difference = 4.64 95% CI: 4.46-4.82, p < 0.00001). Conclusion: This study demonstrated that the effects of nursing care reduced the incidence rate of chemotherapy and the frequency of severe problems in bladder cancer patients.

The divergent response of vegetation phenology to urbanization: A case study of Beijing city, China.

Characterizing the relationship between vegetation phenology and urbanization indicators is essential to understand the impacts of human activities on urban ecosystems. In this study, we explored the response of vegetation phenology to urbanization in Beijing (China) during 2001-2018, using impervious surface area (ISA) and the information of urban-rural gradients (i.e., concentric rings from the urban core to surrounding rural areas) as the urbanization indicators. We found the change rates of vegetation phenology in urban areas are 1.3 and 1.1 days per year for start of season (SOS) and end of season (EOS), respectively, about three times faster than that in forest. Moreover, we found a divergent response of SOS with the increase of ISA, which differs from previous results with advanced SOS in the urban environment than surrounding rural areas. This might be attributed to the mixed land cover types and the thermal environment caused by the urban heat island in the urban environment. Similarly, a divergent pattern of phenological indicators along the urban-rural gradient shows a non-linear response of vegetation phenology to urbanization. These findings provide new insights into the complicated interactions between vegetation phenology and urban environments. High-resolution weather data are required to support process-based vegetation phenology models in the future, particularly under different global urbanization and climate change scenarios.

Inhibition of miR-22 promotes differentiation of osteoblasts and improves bone formation via the YWHAZ pathway in experimental mice.

INTRODUCTION: In senile osteoporosis countering the age-mediated bone loss, promotion of osteoblastogenesis and identification of responsible micro-RNA (miR) would be a successful strategy. MATERIAL AND METHODS: miR microarray screening was carried out to identify the suppressed miRs after real time polymerase chain reaction (RT-PCR) analysis in mesenchymal stem cells (MSCs) derived from adult bone marrow during the proliferation to the mineralization stage. The primary calvarial pre-osteoblasts (human) were harvested and received transfection of miR-22's antagomir or agomir in vitro. Bioinformatics study suggested YWHAZ as the favorable target gene. Next, YWHAZ knockdown was studied for its effect on differentiation of osteoblasts. For in vivo studies, ovariectomized or sham mice were injected with miR-22's antagomir for a period of 6 weeks. The stromal cells were isolated in the 6th week for ex vivo experiments. RESULTS: miR-22 was found to be down-regulated in bone marrow derived mesenchymal stem cells. miR-22's antagomir converted the pre-osteoblasts to a more differentiated and mineralized phenotype showing upregulated protein expression of COL1A1, ALP and CBFA1. The miR-22's antagomir suppressed YWHAZ, enhanced stability of CBFA1 and promoted the differentiation of osteoblasts. In vivo, miR-22's antagomir promoted mineralization and osteoblastogenesis, elevated bone strength and reversed the ovariectomy mediated bone loss in sham mice. CONCLUSIONS: Inhibition of miR-22 may be a potential target for treating osteoporosis clinically. The findings hence suggest that inhibition of miR-22 may be an effective anabolic therapeutic approach in treating osteoporosis clinically.