Glioblastoma is the most common and most aggressive malignant primary brain tumor in humans, accounting for 52 % of all functional tissue brain tumor cases and 20 % of all intracranial tumors. The typical treatment involves a combination of chemotherapy, radiation, and surgery, whereas it still achieves fairly poor patient survival. Ginsenoside Rh2 has been reported to have a therapeutic effect on some tumors, but its effect on glioblastoma has not been extensively evaluated. Here, we show that ginsenoside Rh2 can substantially inhibit the growth of glioblastoma in vitro and in vivo in a mouse model. Moreover, the inhibition of the tumor growth appears to result from combined effects on decreased tumor cell proliferation and increased tumor cell apoptosis. Further analyses suggest that ginsenoside Rh2 may have its antiglioblastoma effect through inhibition of the epidermal growth factor receptor (EGFR) signaling pathway in tumor cells. In a lose-of-function experiment, recombinant EGFR was given together with ginsenoside Rh2 to the tumor cells in vitro and in vivo, which completely blocked the antitumor effects of ginsenoside Rh2. Thus, our data not only reveal an anti-glioblastoma effect of ginsenoside Rh2 but also demonstrate that this effect may function via inhibition of EGFR signaling in glioblastoma cells.

Impairment of intrinsic plasticity is involved in a range of neurological disorders such as epilepsy. However, how intrinsic excitability is regulated is still not fully understood. Here we report that the epigenetic factor Chromodomain Y-like (CDYL) protein is a critical regulator of the initiation and maintenance of intrinsic neuroplasticity by regulating voltage-gated ion channels in mouse brains. CDYL binds to a regulatory element in the intron region of SCN8A and mainly recruits H3K27me3 activity for transcriptional repression of the gene. Knockdown of CDYL in hippocampal neurons results in augmented Nav1.6 currents, lower neuronal threshold, and increased seizure susceptibility, whereas transgenic mice over-expressing CDYL exhibit higher neuronal threshold and are less prone to epileptogenesis. Finally, examination of human brain tissues reveals decreased CDYL and increased SCN8A in the temporal lobe epilepsy group. Together, our findings indicate CDYL is a critical player for experience-dependent gene regulation in controlling intrinsic excitability.

Purpose The aim of the study was to investigate factors which may predispose patients to early neurological deterioration (END) and explore peripheral biomarkers for the prediction of END in cardiogenic cerebral embolism (CCE) patients. Methods Patients diagnosed with CCE within 24 hr of onset between January 2017 and January 2019 were included in this study. END was defined as an increase of ≥2 on the National Institutes of Health Stroke Scale (NIHSS) or the emergence of new neurological symptoms within 3 days of admission. Binary logistic regression was used to investigate the factors associated with END. Receiver operating characteristic (ROC) curves were then generated to determine the predictive value of the potential biomarkers and the optimal cutoff values. Results Of the 129 (male, 55.81%; mean age 71.85 ± 11.99 years) CCE patients, 55 patients with END were identified. Hemorrhage transformation (HT), coronary heart disease (CHD), diastolic blood pressure, cystatin C levels, NIHSS score, and platelet‐to‐lymphocyte ratio (PLR) at admission were independently associated with END. A peripheral cystatin C level ≥ 1.41 mg/L and a PLR ≥ 132.97 were predictive factors for END in CCE patients. The lymphocyte‐to‐monocyte ratio (LMR) was negatively independently associated with HT, and LMR < 2.31 may predict the occurrence of HT in patients with CCE. Conclusions Of the potential predisposing factors considered, increased cystatin C and PLR were associated with END within 3 days of CCE, and a decreased LMR may have predictive value for HT in CCE patients.

The role of atherosclerosis in ischemic stroke has been intensively investigated in recent years, and lipoprotein (a) [Lp(a)] is found to have roles during the process. The aim of this study was to investigate the relationship between acute ischemic stroke (AIS) and serum Lp(a) levels in the Chinese population. All consecutive patients with first-ever acute ischemic stroke during 2011-2012 were recruited to participate in the study. Serum Lp(a) levels and routine tests were examined in both groups. The National Institutes of Health Stroke Scale (NIHSS) score was assessed on admission blinded to Lp(a) levels. In this study, 181 patients with acute ischemic stroke were included. There was a significant difference in median serum Lp(a) levels between acute ischemic stroke patients and control cases (328 [IQR, 173-554] vs. 145 [IQR, 66-254] mg/L, respectively; P = 0.000). Lp(a) levels increased with increasing severity of stroke as defined by the NIHSS score (P = 0.000). For the entire group, when adjusting for other possible risk factors, an elevated Lp(a) level was an independent risk factor for stroke, and a serum Lp(a) level ≥300 mg/L was associated with a 2.23-fold increase in AIS (P = 0.015). In addition, this association was stronger in male than in female patients. High Lp(a) levels are significantly related to stroke, independent from other traditional and emerging risk factors, suggesting that they may play a role in its pathogenesis. It should be considered as a routine risk factor for stroke in the Chinese population.

No abstract