Two new amides from the seeds of Coix lacryma-jobi var. lacryma-jobi.

Phytochemical investigation of the seeds of Coix lacryma-jobi var. lacryma-jobi resulted in the isolation of eight compounds, including two new structures, coixdines A-B (1-2) and six known compounds (3-8). The structures of these compounds were determined by 1 D and 2 D NMR spectra referring to the literatures, together with HR-MS analysis. Coixdine A and B are first examples of spermidine skeleton in genus Coix. In the present paper, all compounds were evaluated for the cytotoxicity against two cancer cell lines (CT-26 and BxPC-3) in vitro, and none of the compounds exhibited obvious cytotoxic activity. The present investigation suggests that these amides seem to be of great chemotaxonomic value for C. lacryma-jobi.

Cytotoxic 13,28 Epoxy Bridged Oleanane-Type Triterpenoid Saponins from the Roots of Ardisia crispa.

Ardisiacrispin D-F (1-3), three new 13,28 epoxy bridged oleanane-type triterpenoid saponins, together with four known analogues (4-7) were isolated from the roots of Ardisia crispa. The structures of 1-7 were elucidated based on 1D and 2D-NMR experiments and by comparing their spectroscopic data with values from the published literatures. Ardisiacrispin D-F (1-3) are first examples that the monosaccharide directly linked to aglycone C-3 of triterpenoid saponins in genus Ardisia are non-arabinopyranose. In the present paper, all compounds are evaluated for the cytotoxicity against three cancer cell lines (HeLa, HepG2 and U87 MG) in vitro. The results show that compounds 1, 4 and 6 exhibited significant cytotoxicity against Hela and U87 MG cells with IC50 values in the range of 2.2 ± 0.6 to 9.5 ± 1.8 µM. The present investigation suggests that roots of A. crispa could be a potential source of natural anti-tumor agents and their triterpenoid saponins might be responsible for cytotoxicity.

Neutrophil Albumin Ratio is Associated with All-Cause Mortality in Stroke Patients: A Retrospective Database Study.

OBJECTIVE: The novel biomarker, neutrophil percentage-to-albumin ratio (NPAR), as a prognostic tool for inflammation in relation to all-cause mortality for patients afflicted by strokes has yet to be explored. METHODS: Data sets associated with patient files stored within the MIMIC-III V1.4 database were obtained. Data files from 940-patients were obtained for this retrospective analysis. Clinical endpoints were determined to represent a month (30-), three months (90-) and year (365-) all-cause mortality in stroke patients were determined. In order to determine NPAR and clinical endpoint relationships, Cox proportional hazards models were utilized. RESULTS: For all-cause mortality within a 30-day period, in an unadjusted model, the HR (95% CIs) in group B (NPAR 20.5-25.0) and C (NPAR >25.0) was 1.17 (0.85, 1.63) and 1.55 (1.13, 2.11) compared with group A (NPAR < 20.5). Proceeding adjustment for more confounding factors, higher NPAR still obtained significant predictive power for 30-day all-cause mortality (HR= 1.45, 95% CI: 1.05, 2.00). Statistical significance (P = 0.0196) was also observed for the other time-based subgroupings for all-cause mortality. CONCLUSION: A strong correlation was present between increased levels of the novel biomarker NPAR and increased risk of mortality in stroke patients.

S100B promotes microglia M1 polarization and migration to aggravate cerebral ischemia.

AIM AND OBJECTIVE: S100B has been found abundantly expressed in microglia during cerebral ischemia. However, S100B effects on phenotype changes and migration of microglia are unclear. METHODS: Real-time PCR of S100B, M1 and M2 markers were tested to characterize phenotypic changes in microglia in mice middle cerebral artery occlusion (MCAO) model. Migration assay and additional mechanism studies were performed to elucidate the role of NF-κB in S100B-mediated microglia M1/M2 phenotype change and migration. Finally, S100B treatment on MCAO models was performed to show the in vivo evidence. RESULTS: S100B was identified as an induced gene with its pattern in accordance with M1 markers in mice MCAO model. That S100B was promoted by M1 stimuli whereas inhibited by M2 stimuli further confirmed S100B a M1 marker. Moreover, S100B promotes microglia M1 polarization with enhanced migration ability and inhibits M2 polarization. Additionally, NF-κB is essential in S100B control in microglia M1/M2 polarization and migration. Furthermore, S100B aggravated cerebral ischemia in murine MCAO model and exacerbated the microglia M1 polarization and migration. CONCLUSIONS: Our findings demonstrate that S100B promotes microglia M1 polarization to aggravate cerebral ischemia, and provide a better understanding on the therapeutic effects of S100B and/or its antagonist/neutralization antibody in stroke.

Low-dosage of rituximab in Chinese patients with neuromyelitis optica spectrum disorder.

Rituximab has been effectively used for treating neuromyelitis optica spectrum disorder (NMOSD) for several years. However those regimens exert a heavy burden on Chinese patients. The aim of our study was to investigate an effectiveness, economic alternatives of RTX. The enrolled patients received different immunosuppressant drugs. Annual relapse rate (ARR), neurological disability (Expanded Disability Status Scale, EDSS), time to the next relapse were evaluated after treatments. Fourteen patients treated with RTX and 37 relapse events from 23 patients treated with traditional immunosuppressant drugs (ISDs) were analyzed in our study. Patients with NMOSD treated with RTX showed a reduction in ARR (2.0 ±â€¯1.8 to 0.2 ±â€¯0.3, p = 0.002) and improve disability (EDSS: 3.7 ±â€¯2.1 to 2.3 ±â€¯2.3, p < 0.001) at last follow-up. Kaplan-Meier analysis indicated that patients treated with RTX had a longer time to next relapse compared with those who were treated with traditional ISDs. Our regimens of RTX treatment were effective in NMOSD patients, and exerted a lower risk of adverse events might be lower than did the high-dose RTX regimens. Moreover, our regimen provides an economic and convenient alternative for NMOSD patients.