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Monoon laui (Merr.) B. Xue and R.M.K. Saunders 2012 is produced in Hainan province. The trunk is straight, the wood texture is straight, and the material is slightly soft, which is suitable for furniture and building materials. In our study, we report and characterize the complete plastome of M. laui The complete length of the plastome of M. laui possesses 161,181 bp, including a large single-copy (LSC) of 89,556 bp, small single-copy (SSC) of 18,977 bp, and two inverted repeats (IRs) of 26,313 bp. The overall G/C content in the plastome of M. laui is 39.13%. The plastome contains 257 genes, consisting of 130 protein-coding genes (16 of which are duplicated in the IR), 37 tRNA genes (seven of which are duplicated in the IR), and eight rRNA genes (5S rRNA, 4.5S rRNA, 16S rRNA, and 23S rRNA). Here, we explore the phylogenetic relationships and make contributions to the conservation genetics of the specie of M. laui using the complete plastome sequence. [ABSTRACT FROM AUTHOR]

Background: Cancer survivors face elevated risks of heart failure (HF) and death, with cardiac dysfunction being a significant concern. Current evaluations often emphasize systolic function while insufficiently addressing diastolic function. This study aims to investigate the prevalence of diastolic dysfunction and assess its prognostic implications in long-term cancer survivors. Methods: We analyzed participants from the Atherosclerosis Risk in Communities (ARIC) Study with complete echocardiographic assessments and documented cancer histories. Diastolic function was classified by guideline criteria: normal (≤ 1 abnormal parameter), indeterminate (2 abnormal parameters), and dysfunction (≥ 3 abnormal parameters). The primary outcomes were incident HF and all-cause death. Diastolic dysfunction prevalence was compared between cancer survivors and non-cancer participants after propensity score matching. Cox regression, Kaplan–Meier, and restricted cubic spline (RCS) analyses were used to assess associated risks. Results: A total of 5322 participants were included, with 18.4% (N = 979) being cancer survivors. The mean age of cancer survivors at echocardiography was 76.3 (5.10) years, with a median of 12.17 years since diagnosis. There were no significant differences in diastolic dysfunction prevalence (12.26% vs 10.73%, P = 0.29) after matching. Cox regression revealed a graded association between diastolic dysfunction and risks of HF and death. Fully adjusted hazard ratios were 2.59 (95% CI: 1.59–4.20, P < 0.001) for indeterminate diastolic function and 4.41 (95% CI: 2.40–8.12, P < 0.001) for diastolic dysfunction in HF; and 1.68 (95% CI: 1.26–2.25, P < 0.001) for indeterminate and 2.21 (95% CI: 1.51–3.22, P < 0.001) for diastolic dysfunction in all-cause death. These results were consistent across subgroup and sensitivity analyses and supported by Kaplan–Meier curves. RCS analyses demonstrated dose–response relationships between individual diastolic parameters and outcomes. Conclusions: Diastolic dysfunction is prevalent among long-term cancer survivors and is stepwise associated with adverse outcomes. These findings underscore the essential need for ongoing monitoring of diastolic function in this population. [ABSTRACT FROM AUTHOR]

With the acceleration of urbanization, urban traffic congestion is becoming more and more serious, in which the timing of signal lights for regional traffic optimization is particularly important. Since existing signal lights-based traffic optimization technologies, especially green wave, do not take the regional traffic follow into consideration, therefore not being efficient. Therefore, we propose Adaptive Signal Light Timing for Regional Traffic Optimization based on Graph Convolutional Network Empowered Traffic Forecasting. First, we propose a multi-intersection traffic flow prediction model, namely, A-GCN + with an improved prediction accuracy of 6.3%, which utilizes the attention-aggregated graph convolutional neural networks (A-GCN) and temporal convolutional networks (TCN) to extract spatial and temporal features of the traffic flow. Second, we propose a dynamic regional traffic signal coordination optimization control method, which utilizes the predicted intersection approach traffic flow from A-GCN + and combines it with the improved whale optimization algorithm (IWOA) to obtain the optimal solution for the regional average vehicle delay model. Finally, we propose a bidirectional green wave automatic control method for the main line, which utilizes the optimized results of dynamic regional traffic signal timing and employs a multi-strategy fusion graphical method to obtain the dynamic main line bidirectional green wave. Experimental results show that compared to the traditional graphical method, the multi-strategy fusion graphical method increases the green wave bandwidth by 20%. The mainline bidirectional green wave adaptive coordinated control method improves main line traffic efficiency by 32.3% and regional network traffic efficiency by 8.7%. • A cross-intersection traffic flow prediction model A-GCN+ utilizing Attention-aggregated GCN and TCN for TS features. • A dynamic regional traffic signal coordination method with improved whale optimization algorithm and results of A-GCN+. • A bidirectional green wave automatic control method with a multi-strategy fusion graphical method for the main line. • The multi-strategy fusion graphical method increases the green wave bandwidth by up to 20%. • The proposed method improves main line traffic efficiency by 32.3% and regional network traffic efficiency by 8.7%. [ABSTRACT FROM AUTHOR]

Mitochondrial dysfunction and metabolic reprogramming are key features of hepatocellular carcinoma (HCC). Despite its significance, the precise underlying mechanism behind these processes has not been fully elucidated. The latest investigations, along with our previous discoveries, have substantiated the significant role of mitochondrial ribosomal protein L12 (MRPL12), a newly identified gene involved in mitochondrial transcription regulation, in the modulation of mitochondrial metabolism. Nevertheless, the role of MRPL12 in tumorigenesis has yet to be investigated. The expression of MRPL12 in HCC was assessed using an online database. Western blot, quantitative real-time polymerase chain reaction (qRT-PCR), and immunohistochemistry (IHC) were employed to determine the expression of MRPL12 in HCC tissues, patient-derived organoid (PDO), and cell lines. The correlation between MRPL12 expression and clinicopathological features, as well as prognosis, was examined using tissue microarray analysis. An in vivo subcutaneous tumor xenograft model, gene knockdown or overexpression assay, chromatin immunoprecipitation (ChIP) assay, Seahorse XF96 assay, and cell function assay were employed to investigate the biological function and potential molecular mechanism of MRPL12 in HCC. A significant upregulation of MRPL12 was observed in HCC cells, PDO and patient tissues, which correlated with advanced tumor stage, higher grade and poor prognosis. MRPL12 overexpression promoted cell proliferation, migration, and invasion in vitro, as well as tumorigenicity in vivo, whereas MRPL12 knockdown showed the opposite effect. MRPL12 knockdown also inhibited the capacity of organoids proliferation capacity. Furthermore, MRPL12 was found to be crucial for maintaining mitochondrial homeostasis. Both gain and loss-of-function experiments targeting MRPL12 in HCC cells altered oxidative phosphorylation (OXPHOS) and mitochondrial DNA content. Notably, suppression of OXPHOS effectively mitigates the tumor-promoting effect attributed to MRPL12 overexpression, implying the involvement of MRPL12 in HCC through the modulation of mitochondrial metabolism. Besides, Yin Yang 1 (YY1) was identified as a transcription factor responsible for regulating MRPL12, while the PI3K/mTOR pathway was found to act as an upstream regulator of YY1. MRPL12 knockdown attenuated the YY1 overexpression or PI3K/mTOR activation-induced malignant phenotype in HCC cells. Our findings provide compelling evidence that MRPL12 is implicated in driving the malignant phenotype of HCC via regulating mitochondrial metabolism. Moreover, the aberrant expression of MRPL12 in HCC is mediated by the upstream PI3K/mTOR/YY1 pathway. These results highlight the potential of targeting MRPL12 as a promising therapeutic strategy for the treatment of HCC. Graphical illustration of mechanism in HCC progress. MRPL12 is implicated in driving the malignant phenotype of HCC via regulating mitochondrial metabolism. The MRPL12 upregulation in HCC is mediated by the upstream PI3K/mTOR/YY1 pathway. [Display omitted] • MRPL12 is upregulated in HCC tissues, patient-derived organoid, and cell lines. • MRPL12 is correlated with advanced tumor stage, higher grade and poor prognosis. • MRPL12 is involved in maintain mitochondrial homeostasis in HCC. • MRPL12 promotes HCC tumorigenicity via reprogramming mitochondrial metabolism. • MRPL12 is regulated by PI3K/mTOR/YY1 pathway. [ABSTRACT FROM AUTHOR]