During chemotherapy for lymphoma, the administration of cytotoxic agents and rituximab often results in hepatitis B reactivation (incidence, 14-72%). This study was designed to compare the efficacy of entecavir and lamivudine in preventing hepatitis B reactivation in lymphoma patients. Between January 2007 and February 2009, patients treated in four hospitals in China were screened to identify those most appropriate for analysis. These patients received either entecavir or lamivudine during chemotherapy and for 6 months after completion of chemotherapy. A total of 34 patients received entecavir and 89 patients received lamivudine. Compared with the lamivudine group, the entecavir group had significantly lower rates of hepatitis (5.9 vs 27.0%, P = 0.007), hepatitis B reactivation (0 vs 12.4%, P = 0.024) and disruption of chemotherapy (5.9 vs 20.2%, P = 0.042). All patients with hepatitis B reactivation had B-cell non-Hodgkin's lymphoma (stage III-IV). In lymphoma patients under chemotherapy treatment, entecavir is more effective than lamivudine in preventing hepatitis B reactivation. For patients with advanced stage disease, entecavir should be considered the primary preventive therapy.

What is the central question of this study? We investigated the potential neuroprotective effects of catechin after traumatic brain injury and explored the underlying mechanisms. What is the main finding and its importance? Catechin treatment had neuroprotective effects in a rat model of traumatic brain injury, and these effects might be mediated by intervention in the self-perpetuating process of blood-brain barrier disruption and excessive inflammatory reaction. Traumatic brain injury (TBI) resulting from external force on the head usually leads to long-term deficits in motor and cognitive functions. Catechin has shown neuroprotective effects in neurodegenerative diseases and ischaemia models. We therefore investigated the potential neuroprotective effects of catechin after TBI and explored the underlying mechanisms. Male rats were subjected to controlled cortical impact injury and then treated with catechin. Brain damage, motor and cognitive functions, blood-brain barrier (BBB) integrity and neuro-inflammation were examined. Catechin treatment ameliorated brain damage and motor and cognitive deficits after TBI. Catechin was shown to protect BBB integrity, alleviate the TBI-induced loss of the junction proteins occludin and zonula occludens protein-1 and suppress local inflammatory reactions. Catechin treatment had neuroprotective effects in a rat model of TBI, and these effects might be mediated by intervention in the self-perpetuating process of BBB disruption and excessive inflammatory reaction.

Background: Gastric cancer (GC) is one of the most lethal cancers worldwide with a high risk for recurrence and metastasis. Therefore, further understanding of the metastatic mechanism and the development of treatment strategies are required. Although increasing evidence suggests that SWI/SNF Related, Matrix Associated, Actin Dependent Regulator of Chromatin, Subfamily E, Member 1 (SMARCE1) promotes cancer metastasis, its role in GC remains unclear. Materials and methods: GC samples (n=122) were used to investigate the association between SMARCE1 expression, patient clinicopathological features, and prognosis. The expression of SMARCE1 in GC tissues was measured using real-time polymerase chain reaction, western blotting, and immunohistochemistry. MGC-803 and AGS cells were transfected with lentivirus to upregulate or downregulate SMARCE1 expression. The roles of SMARCE1 in GC cell proliferation, migration, and invasion were determined using Cell Counting Kit-8 assay, colony formation assay, wound healing, transwell migration, and invasion assay. Nude mice models were established to observe tumorigenesis. The specific mitogen-activated protein kinase (MAPK) inhibitor U0126 was utilized to verify the involved pathway. Results: SMARCE1 was highly expressed in GC tissues and cell lines. High expression of SMARCE1 was correlated with the malignant clinicopathological characteristics of GC patients, including tumor size, depth of invasion, degree of differentiation, lymph node involvement, and TNM stage (all P <0.05). Kaplan–Meier survival analysis revealed that high SMARCE1 expression predicted poor prognosis in GC patients ( P <0.01). Moreover, SMARCE1 was an independent risk factor of poor prognosis ( P <0.01). Functional study revealed that overexpression of SMARCE1 markedly promoted the proliferation, migration, and invasion of GC cells in vitro and tumorigenesis in vivo. Furthermore, SMARCE1 activated the MAPK/ERK signaling pathway. U0126 significantly inhibited the SMARCE1-induced proliferation and mobility of GC cells. Conclusion: SMARCE1 promoted growth and metastasis of GC, indicating its potential usefulness as a prognostic biomarker and target for therapeutic intervention against this disease.

Background:Long noncoding RNAs have been shown to play crucial roles in cancer biology, while the long noncoding RNA landscapes of pancreatic ductal adenocarcinoma have not been completely characterized. We aimed to determine whether long noncoding RNA could serve as early diagnostic biomarkers for pancreatic ductal adenocarcinoma.Method:We conducted a genome-wide microarray analysis on pancreatic ductal adenocarcinoma and their adjacent noncancerous tissues from 8 Chinese patients.Results:A total of 3352 significantly differentially expressed long noncoding RNAs were detected. Of total, 1249 long noncoding RNAs were upregulated and 2103 were downregulated (fold change ≥2, P < 0.05, FDR <0.05). These differentially expressed long noncoding RNAs were not evenly distributed among chromosomes in human genome. Hierarchical clustering of these differentially expressed long noncoding RNAs revealed large variabilities in long noncoding RNA expression among individual patient, indicating that certain long noncoding RNAs could play a unique role or be used as a biomarker for specific subtype of pancreatic ductal adenocarcinoma. Gene Ontology enrichment and pathway analysis identified several remarkably dysregulated pathways in pancreatic ductal adenocarcinoma tissue, such as interferon-γ-mediated signaling pathway, mitotic cell cycle and proliferation, extracellular matrix receptor interaction, focal adhesion, and regulation of actin cytoskeleton. The co-expression network analysis detected 393 potential interactions between 80 differentially expressed long noncoding RNAs and 105 messenger RNAs. We experimentally verified 7 most markedly dysregulated long noncoding RNAs from the network.Conclusion:Our study provided a genome-wide survey of dysregulated long noncoding RNAs and long noncoding RNA/messenger RNA co-regulation networks in pancreatic ductal adenocarcinoma tissue. These dysregulated long noncoding RNA/messenger RNA networks could be used as biomarkers to provide early diagnosis of pancreatic ductal adenocarcinoma or its subtype, predict prognosis, and evaluate treatment efficacy.