Background and Purpose-Motor weakness progression is relatively common in acute pontine infarction and frequently associated with increased functional disability. We designed this study to identify the predictors of progression of motor weakness in patients with pontine infarction during the acute phase. Methods-We identified consecutive patients with acute ischemic stroke in the pons. Patients were defined as having progressive motor deficits (PMD) if their motor National Institutes of Health Stroke Scale scores increased by Ն1 unit between the maximal and initial neurological deficits. To define the predictors of PMD in patients with a pontine infarct, clinical, laboratory, diffusion-weighted imaging lesion location, and magnetic resonance angiographic variables were investigated. Results-A total of 190 patients (male:femaleϭ112:78, 66.4Ϯ10.6) were identified, and 49 (25.8%) patients were diagnosed with progressive motor deficits. Logistic multiple regression analysis identified lesion involvement of the lower pons (odds ratio, 3.768; 95% confidence interval, 1.696 -8.371) as an independent risk factor contributing to motor progression. Although 34 patients (17.9%) had significant basilar artery stenosis, there was no relationship between PMD in pontine infarct patients and the presence of basilar artery stenosis. Additionally, female and previous hypertension were associated with PMD (odds ratio, 2.651, 95% confidence interval, 1.211-5.802; odds ratio, 3.051, 95% confidence interval, 1.087-9.673). Conclusions-Our results suggest that lower pons lesions may contribute to progressive motor deficits in patients with isolated acute pontine infarction. Infarct topography is therefore a potential prognostic factor of PMD, because the location of the infarct can affect the extent of ischemic degeneration of the corticospinal tract. (Stroke. 2012;43: 708-713.)

A new sinapoyl glycoside, 1,3-di-O-sinapoyl-β-D-glucopyranose (1) along with 13 known compounds, including, sinapoyl glycosides (2 and 3), cardenolide glycoside (4), flavonoids (5-10), lignan (11), phenolic acids (12 and 13), and phytosterol (14), were isolated from the seeds of Descurainia sophia by chromatographic separation methods. The structures of 1-14 were determined by the interpretation of spectroscopic data as well as by comparison of that data with previously reported values. Compounds 2, 3, 5, 6, and 11 were identified in and isolated from this plant for the first time in this study. All isolates were evaluated for in vitro cytotoxic activities against seven human cancer cell lines and for in vitro anti-inflammatory potential using LPS-stimulated RAW264.7 murine macrophages. Compound 4 showed potent cytotoxicity (IC50 values ranging from 0.034 to 0.596 μM) against all human cancer cell lines tested and was identified as the main active cytotoxic constituent of this plant. Compound 8 (ED50 = 5.45 μM) and 11 (ED50 = 10.02 μM) exerted dose-dependent inhibitory effects on NO production in LPS-stimulated RAW264.7 cells.

BackgroundGleditsia sinensis thorns have been widely used in traditional Korean medicine for the treatment of several diseases, including obesity, thrombosis, and tumor-related diseases. The aim of the study is to determine the antiangiogenic effect of Gleditsia sinensis thorns in vitro and in vivo in a bid to evaluate its potential as an anticancer drug.MethodsEthanol extract of Gleditsia sinensis thorns (EEGS) were prepared and used for in vitro and in vivo assays. In vitro antiangiogenic effect of EEGS was determined in HUVEC primary cells by cell migration and tube formation assays. In vivo antiangiogenic effect of EEGS was determined by measuring vessel formation and vascular endothelial cells migrating into the implanted matrigels in nude mice. The angiogenesis-related proteins of which expression levels were altered by EEGS were identified by proteomic analysis.ResultsEEGS exerted a dose-dependent antiproliferative effect on HUVEC cells without significant cytotoxicity. Angiogenic properties, such as cell migration and tube formation, were significantly inhibited by EEGS in a dose-dependent manner. New vessel formation was also suppressed by EEGS, as determined by the directed in vivo angiogenesis assays in nude mice. EEGS reduced the expression of proangiogenic proteins, endothelin 1 and matrix metallopeptidase 2, in HUVEC cells.ConclusionsOur findings suggest that EEGS can inhibit angiogenesis by down-regulating proangiogenic proteins, and therefore it should be considered as a potential anticancer drug targeting tumor-derived angiogenesis.

Aim: To investigate the immunoregulatory functions of water extracts of Hericium erinaceum (WEHE) focusing on natural killer (NK) cell-based anticancer activities. Methods: Mouse splenocytes or purely isolated NK cells were stimulated with 1-100 mg/L WEHE for 24 h followed by co-culture with 51 Cr-labled Yac-1 cells for 4 h, then NK cell-derived cytolytic activity was measured using a radio-release assay. Neutralizing antibodies against mouse interleukin-12 (IL-12) were added into the WEHE-stimulated splenocytes, thereafter, cytotoxicity was measured to examine the involvement of IL-12. RT-PCR and ELISA analyses were performed to confirm the induction of transcription and the translation of IL-12 and interferongamma (IFN-gamma) in the WEHE-treated splenocytes. Results: WEHE enhanced the cytolytic activity of total splenocytes towards Yac-1 cells in a dose-dependent manner. However, this activation was not observed when the NK cells isolated from the splenocytes were treated with WEHE. Furthermore, the treatment with antibodies against IL-12 abolished the effect of WEHE on splenocyte-derived cytolytic activity. RT-PCR and ELISA analyses showed the induction of IL-12 and IFN-gamma in the WEHE-treated splenocytes. Conclusion: WEHE indirectly activates the cytolytic ability of NK cells via the induction of IL-12 in total splenocytes, and possibly via other immuno-mediators or cellular components.