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Alzheimer’s disease (AD) is a progressive and degenerative disorder accompanied by cognitive decline, which could be promoted by mitochondrial dysfunction induced by mitochondrial Ca 2+ (mCa 2+) homeostasis Mitochondrial calcium uniporter (MCU), a key channel of mCa 2+ uptake, may be a target for AD treatment. In the present study, we reveal for the first time that MCU knockdown in hippocampal neurons improves the memory performance of APP/PS1/tau mice through radial arm maze task. Western blot analysis, transmission electron microscopy (TEM), Golgi staining, immunohistochemistry (IHC) and ELISA results demonstrate that MCU knockdown in hippocampal neurons upregulates the levels of postsynaptic density protein 95 (PSD95) and synaptophysin (SYP), and increases the numbers of synapses and dendritic spines. Meanwhile, MCU knockdown in hippocampal neurons decreases the neuroinflammatory response induced by astrogliosis and high levels of IL-1β and TNF-α, and improves the PINK1-Parkin mitophagy signaling pathway and increases the level of Beclin-1 but decreases the level of P62. In addition, MCU knockdown in hippocampal neurons recovers the average volume and number of mitochondria. These data confirm that MCU knockdown in hippocampal neurons improves the memory performance of APP/PS1/tau mice through ameliorating the synapse structure and function, relieving the inflammation response and recovering mitophagy, indicating that MCU inhibition has the potential to be developed as a novel therapy for AD.

With the increasing number of cancer patients, how to care for cancer survivors and establish a sound cancer survivorship care model has become a hot topic in China and even the world. The development of cancer survivorship care model in China is still in its infancy. There are some deficiencies in cancer care and the management needs to be improved. We reviewed the latest developments in foreign cancer care models, and analyzed the aspects that merit attention, such as care process improvement, resource convergence and model innovation, then based on current situation of cancer care in China, we advised from five aspects to facilitate domestic development of cancer survivorship care models: using tiered diagnosis and treatment to individualizedly manage cancer survivors, developing and improving cancer care guidelines, building a strong cancer care workforce, innovating cancer care management, and strengthening policy and institutional measures to reduce the cancer burden.

In view of China's "carbon peak, carbon neutral" strategy, especially the important point of reaching the carbon peak by 2035 and achieving socialist modernisation, it is important to select a number of priority end-use energy consumption technology topics to promote the company's technological innovation. Based on the results of the two rounds of the Delphi survey, eight end-use energy consumption technologies with a "dual carbon" focus should be prioritised, namely: virtual power plant technology, electric vehicle technology, impact assessment and costing of carbon emissions and reduction, and carbon dioxide capture and storage technology. The results of the Delphi survey show that R&D investment, policy mechanisms and market viability are the main constraints to the completion of these technologies. In response to these constraints, relevant recommendations are made in terms of funding input, institutional development and market development.

Soil organic matter (SOM) content is an effective indicator of desertification; thus, monitoring its spatial‒temporal changes on a large scale is important for combating desertification. However, mapping SOM content in desertified land is challenging owing to the heterogeneous landscape, relatively low SOM content and vegetation coverage. Here, we modeled the SOM content in topsoil (0–20 cm) of desertified land in northern China by employing a high spatial resolution dataset and machine learning methods, with an emphasis on quarterly green and non-photosynthetic vegetation information, based on the Google Earth Engine (GEE). The results show: 1) the machine learning model performed better than the traditional multiple linear regression model (MLR) for SOM content estimation, and the Random Forest (RF) model was more accurate than the Support Vector Machine (SVM) model; 2) the quarterly information regarding green vegetation and non-photosynthetic were identified as key covariates for estimating the SOM content in desertified land, and an obvious improvement could be observed after simultaneously combining the Dead Fuel Index (DFI) and Normalized Difference Vegetation Index (NDVI) of the four quarters (R2 increased by 0.06, the root mean square error decreased by 0.05, the ratio of prediction deviation increased by 0.2, and the ratio of performance to interquartile distance increased by 0.5). In particular, the effects of the DFI in Q1 (the first quarter) and Q2 (the second quarter) on estimating low SOM content (

Objective: microRNA‐450b (miR‐450b) plays an important role in cancer progression; however, its function in oral squamous cell carcinoma (OSCC) remains largely unknown. This study aimed to investigate the action mechanisms of miR‐450b in OSCC. Materials and Methods: OSCC animal model was established via continuous induction with single‐drug 7, 12‐dimethylbenzo[a]anthracene (DMBA). Animal tissue samples were pathologically typed using haematoxylin–eosin (HE) staining. The Cancer Genome Atlas (TCGA) database was used to predict miR‐450b and SERPINB2 expression in head and neck squamous cell carcinoma (HNSCC). qRT‐PCR and Western blotting were used to detect gene and protein expression in OSCC tissue and cells, respectively. OSCC cell proliferation, growth, migration and invasion were detected using CCK‐8, colony formation, transwell migration and matrigel invasion assays, respectively. Bioinformatic tools were used to predict miR‐450b target genes. Dual‐luciferase reporter assay was used to verify targeting between miR‐450b and SERPINB2. Finally, small interfering RNA (siRNA) was used to reduce SERPINB2 expression to detect its effect on tumourigenesis. Results: Four stages of OSCC carcinogenesis (normal oral epithelium, simple epithelial hyperplasia, dysplasia and OSCC) were identified. miR‐450b was found to be overexpressed in OSCC animal samples, HNSCC samples and human OSCC cells. Upregulation of miR‐450b significantly promoted OSCC cell proliferation, colony formation, migration and invasion, while its downregulation had the opposite effect. SERPINB2 was found to be a miR‐450b target gene, and its expression was negatively correlated with miR‐450b expression. Altering SERPINB2 expression effectively inhibited OSCC cell invasion, metastasis and epithelial‐mesenchymal transition (EMT). Conclusions: miR‐450b plays a key role in OSCC tumourigenesis by regulating OSCC cell migration, invasion and EMT via SERPINB2. [ABSTRACT FROM AUTHOR]

Background: The CRISPR/Cas9 system is widely used for genome editing in human, rat and mouse cells. In this study, we established Fzd6 mutant mice using CRISPR/Cas9 technology, and obtained Fzd6 homozygous mutant (Fzd6Q152E) mice through breeding. Fzd6 plays a role in depression, but there are few related reports. We used this model to investigate the mechanism of Fzd6 involved in depression, and build a solid foundation for subsequent in-depth studies. Methods and Results: The target of Fzd6 mutation was obtained by CRISPR/Cas9 technology and hippocampal tissue was collected for Nissl staining and histological analysis. Blood was collected for enzyme linked immunosorbent assay (ELISA); The gene expression of Fzd6 and the related genes expression in wnt pathway was quantified by quantitative real-time PCR (qRT-PCR), and then expression of Fzd6 and proteins in the Wnt pathway were identified by western blotting. ELISA results showed that the expression levels of brain derived neurotrophic factor (BDNF), 5-hydroxytryptamine (5-HT), and Noradrenaline (NE) in serum were significantly decreased in Fzd6Q152E mice, whereas the mRNA expression of Lrp5, Lrp6, and Dkk2 is increased. The western blotting revealed that the expression of Fzd6 and Lrp6 is decreased, although the expression of Dkk2 and Gsk-3β increased. Conclusion: Our study successfully established homozygous Fzd6 mutant mice model. The relationship between Fzd6-Wnt and depression was preliminarily clarified, which provides an ideal animal model for subsequent research on diseases induced by the Fzd6 mutation. [ABSTRACT FROM AUTHOR]