This is the chromosome-level genome assembly and annotations of Scyphiphora hydrophylacea. If you use this dataset, please cite the following publication:
Li, Y., Shao, S., Zhu, R., Wang, Y., Jin, C., Liu, M., Huang, K., Guo, Z., He, Z., Shi, S. and Xu, S. (2025), Tandem gene duplication facilitates intertidal adaptation in atypical mangrove plants. Plant J, 123: e70456. https://doi.org/10.1111/tpj.70456

Background: Pro-inflammatory cytokines may be associated with post-stroke depression (PSD); however, results from different studies are inconsistent. Objectives: To investigate whether pro-inflammatory cytokines are associated with the development of PSD in acute stroke. Methods: PubMed, Embase, and Web of science were searched for relevant literature. Meta-analyzes were performed to determine whether the baseline blood concentrations of pro-inflammatory cytokines differed between acute stroke patients with and without depression. Sensitivity analyzes and regression analyzes were conducted to explore sources of heterogeneity. Results: We included 889 acute stroke patients from eight original studies, 312 of whom developed PSD and 577 did not. The serum concentrations of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) were higher in the PSD group, compared with the non-PSD group (IL-6: SMD = 1.26, 95% CI = [0.55, 1.97], P < 0.001; TNF-α: SMD = 0.61, 95% CI = [0.13, 1.10], P = 0.010). Conclusions: This study indicates IL-6 and TNF-α as potential biomarkers of PSD in the acute stage of stroke and provides theoretical support for the early prevention and treatment of PSD.

The initial and final logistic models of binary logistic regression analysis of burnout. (XLS 41 kb)

The initial and final logistic models of binary logistic regression analysis of burnout. (XLS 41 kb)

Breast cancer stem cells (BCSCs) have the greatest potential to maintain tumorigenesis in all subtypes of tumor cells and were regarded as the key drivers of tumor. Recent evidence has demonstrated that BCSCs contributed to a high degree of resistance to therapy. However, how BCSCs self renewal and tumorigenicity are maintained remains obscure. Herein, our study illustrated that overexpression of let-7a reduced cell proliferation and mammosphere formation ability of breast cancer stem cells(BCSCs) in a KRas-dependent manner through different pathways in vitro and in vivo. To be specific, we provided the evidence that let-7a was decreased, and reversely the expression of KRas was increased with moderate expression in early stages (I/II) and high expression in advanced stages (III/IV) in breast cancer specimens. In addition, the negative correlation between let-7a and KRas was clearly observed. In vitro, we found that let-7a inhibited mammosphere-forming efficiency and the mammosphere-size via NF-κB and MAPK/ERK pathway, respectively. The inhibitory effect of let-7a on mammosphere formation efficiency and the size of mammospheres was abolished after the depletion of KRas. On the contrary, enforced expression of KRas rescued the effect of let-7a. In vivo, let-7a inhibited the growth of tumors, whereas the negative effect of let-7a was rescued after overexpressing KRas. Taken together, our findings suggested that let-7a played a tumor suppressive role in a KRas-dependent manner.

Breast cancer stem cells (BCSCs) have the greatest potential to maintain tumorigenesis in all subtypes of tumor cells and were regarded as the key drivers of tumor. Recent evidence has demonstrated that BCSCs contributed to a high degree of resistance to therapy. However, how BCSCs self renewal and tumorigenicity are maintained remains obscure. Herein, our study illustrated that overexpression of let-7a reduced cell proliferation and mammosphere formation ability of breast cancer stem cells(BCSCs) in a KRas-dependent manner through different pathways in vitro and in vivo. To be specific, we provided the evidence that let-7a was decreased, and reversely the expression of KRas was increased with moderate expression in early stages (I/II) and high expression in advanced stages (III/IV) in breast cancer specimens. In addition, the negative correlation between let-7a and KRas was clearly observed. In vitro, we found that let-7a inhibited mammosphere-forming efficiency and the mammosphere-size via NF-κB and MAPK/ERK pathway, respectively. The inhibitory effect of let-7a on mammosphere formation efficiency and the size of mammospheres was abolished after the depletion of KRas. On the contrary, enforced expression of KRas rescued the effect of let-7a. In vivo, let-7a inhibited the growth of tumors, whereas the negative effect of let-7a was rescued after overexpressing KRas. Taken together, our findings suggested that let-7a played a tumor suppressive role in a KRas-dependent manner.