Meng Li

Glioblastoma (GBM) is an aggressive brain tumor with a poor prognosis, largely due to the presence of glioblastoma stem cells (GSCs). These cells drive tumor progression, recurrence, and chemoresistance, making them critical targets for therapy. This study aims to identify novel GSC markers for improved diagnosis and targeted treatment. We utilized single-cell RNA sequencing (scRNA-seq) and bulk RNA-seq data to identify PDLIM1 as a novel GSC marker. PDLIM1 was specifically expressed in GSCs and was associated with poor prognosis and advanced tumor stages. Functional assays demonstrated that PDLIM1 overexpression enhanced GBM cell proliferation, reduced apoptosis, increased GSC proportions, and promoted chemoresistance and tumorigenesis. Conversely, PDLIM1 knockdown inhibited these processes. Mechanistically, PDLIM1 was found to exert its effects likely by promoting the PI3K-AKT pathway. In conclusion, PDLIM1 may serve as a potential marker of GSCs associated with poor prognosis, tumorigenesis, and chemoresistance in GBM, representing a potential therapeutic target for improving GBM patient outcomes.

PHD2 is essential in modulating HIF-1α levels upon oxygen fluctuations. Hypoxia, a hallmark of uterus, and HIF-1α have recently emerged as opposing regulators of mesendoderm specification, suggesting a role for PHD2 therein. We found that PHD2 expression initially covered the epiblast and gradually receded from the primitive streak, which was identical to hypoxia and exclusive to HIF-1α. The investigations performed in mESCs, embryoids, and mouse embryos together demonstrated that PHD2 negatively regulated mesendoderm specification. Single-cell RNA sequencing revealed that PHD2 governed the transition from epiblast to mesendoderm. The downstream effect of PHD2 relied on the HIF-1α regulated Wnt/β-catenin pathway, while it was regulated upstream by miR-429. In summary, our research highlights PHD2’s essential role in mesendoderm specification and its interactions with hypoxia and HIF-1α.

Background: To investigate the morphological changes of the whole-brain in patients with alcohol addiction using voxel-based morphometry (VBM). Methods: Twenty alcohol addiction individuals and 20 healthy control volunteers, matched in gender, age, handedness and education, were enrolled as the alcohol addiction group and control group, respectively, from June 2017 to February 2018. The two groups underwent magnetic resonance imaging (MRI) scans of the whole-brain using a 3.0T MRI system, and the MRI images were analyzed by VBM. Total brain volume analysis was performed to observe the changes of local brain volume. Independent samples t-test was used for comparison of whole-brain volumes between the two groups. Results: Gray matter volume (GMV) was significantly more reduced in the left middle frontal gyrus, left superior frontal gyrus, left precuneate gyrus, left gyrus rectus, right medial superior frontal gyrus, and right orbital gyrus in patients with alcohol addiction than in healthy controls. White matter volume (WMV) in the bilateral superior frontal gyrus was also significantly more reduced in patients with alcohol addiction than in healthy controls. Whole-brain VBM results showed that white matter and brain parenchyma volumes (BPVs) were significantly smaller in patients with alcohol addiction than in healthy controls (both P0.05). Conclusions: There are dominant areas of brain atrophy in patients with alcohol addiction. The VBM has a potential application value in detecting subtle brain atrophy in patients with alcohol addiction and providing an imaging basis in the diagnosis of alcohol addiction.