Epidemiological Features of Spinal Cord Injury in China: A Systematic Review

Background: Spinal cord injury (SCI) is a severe condition that disrupts patients' physiological, mental, and social well-being state and exerts great financial burden on patients, their families and social healthcare system. This review intends to compile studies regarding epidemiological features of SCI in China.Methods: Searches were conducted on PubMed, EMBASE, Web of Science and Cochrane Library for relevant studies published through January, 2018. Studies reported methodological and epidemiological data were collected by two authors independently.Results: Seventeen studies met the inclusion criteria. Two studies reported incidence of SCI that is 60.6 in Beijing (2002) and 23.7 in Tianjin (2004–2008). All studies showed male had a larger percentage in SCI compared to female except Taiwan (2000–2003). The average male and female ratio was 3–4:1 in China and the highest male and female ratio was 5.74: 1 in Tianjin (2004–2007). Farmers, laborers and unemployed people accounted for more than half of the SCI patients in China. Fall was the primary causation with exception of Heilongjiang (2009–2013), Beijing (2001–2010), and Taiwan (2002–2003), where motor vehicle collision (MCVs) was the leading causation. Pulmonary infection, urinary tract infection and bedsore were common complications, accounting for approximately 70% of SCI patients in China.Conclusion: This review shows that epidemiological features of SCI are various in different regions in China and prevention should be implemented by regions. The number of patients with SCI result from fall and MCVs may become a main public health problem because population aging and economic developing in China. However, because all included studies were retrospective and lacking a register system in China, some data were incomplete and some cases may be left out, so the conclusion may not be generalizable to the other regions

Luteolin Promotes Cell Apoptosis by Inducing Autophagy in Hepatocellular Carcinoma

Background/Aims: Hepatocellular carcinoma (HCC) is the most common primary liver malignancy and is a leading cause of cancer-related death worldwide. Luteolin, a flavonoid from traditional Chinese medicine, shows anti-cancer activity in many cancer cells, including HCC. However, the mechanism underlying the action of luteolin in HCC, especially its role in regulating cell autophagy, remains unclear. In the present study, we investigated the role of luteolin in regulating cell autophagy and the role of autophagy in luteolin-induced apoptosis. Methods: The 3-(4,5-dimethythiazol-2-yl)-2,5-diphenyl tetrazolium bromide assay (MTT) was used to investigate cell viability. Flow cytometry analysis was used to detect the cell cycle and cell apoptosis. Hoechst 33342 staining was used to detect cell apoptosis. Transmission electron microscopy was used to investigate autophagy. qRT-PCR and western blotting were used to detect apoptosis- and autophagy-related mRNAs and proteins. Results: Luteolin reduced the viability of SMMC-7721 cells in a time and dose-dependent manner, and induced significant G0/G1-phase arrest. In addition, the results of flow cytometry analysis and Hoechst 33342 staining showed that luteolin treatment increased the number of apoptotic cells obviously, and the results of qRT-PCR and western blotting showed that luteolin treatment increased caspase 8 and decreased bcl-2 at the mRNA and protein levels. Furthermore, luteolin increased the number of intracellular autophagosomes, promoted LC3B-I conversion to LC3B-II, and increased Beclin 1 expression. Finally, co-treatment with the autophagy inhibitor chloroquine weakened the effects of luteolin on cell apoptosis. Conclusion: Luteolin induced apoptosis in human liver cancer SMMC-7721 cells, partially via autophagy. Thus, luteolin could be used as a regulator of autophagy in HCC treatment

Identification and Verification of Candidate Genes Regulating Neural Stem Cells Behavior Under Hypoxia

Background/Aims: Neural stem cells (NSCs) reside in a hypoxic environment, and hypoxia plays an important role in their development and differentiation. This study aimed to explore the underlying mechanisms by which hypoxia affects NSC behavior. Methods: In the current study, we downloaded the gene expression dataset GSE68572 and identified the differentially expressed genes (DEGs) by analyzing high-throughput gene expression in hypoxic and normoxic NSCs. Subsequently, we analyzed these data using a combined bioinformatics approach and predicted the microRNAs (miRNAs) targeting the key gene using miRNA databases. Quantitative real-time PCR (qRT-PCR) was used to validate the expression of the top five DEGs. Results: In total, 1347 genes were identified as DEGs. We identified the predominant gene ontology categories and Kyoto Encyclopedia of Genes and Genomes pathways that were significantly over-represented in the hypoxic NSCs. A protein–protein interaction network he identification of miRNAs and their putative targets may offer new diagnostic and therapeutic strategies for liver cancer the top 10 core genes. Vascular endothelial growth factor A (VEGFA) had the highest degree and may be the key gene concerning NSC behavior under hypoxia. Further validation of the top five DEGs by qRT-PCR demonstrated that four DEGs were significantly higher and one DEG was significantly lower in the hypoxic group than in the control group. Seven miRNAs were predicted and proved to target VEGFA. Conclusion: This preliminary study can prompt the understanding of the molecular mechanisms by which hypoxia has an impact on NSC behavior and can help to optimize stem cell therapies for central nervous system injuries and diseases

Proteogenomics of clear cell renal cell carcinoma response to tyrosine kinase inhibitor

Abstract The tyrosine kinase inhibitor (TKI) Sunitinib is one the therapies approved for advanced renal cell carcinoma. Here, we undertake proteogenomic profiling of 115 tumors from patients with clear cell renal cell carcinoma (ccRCC) undergoing Sunitinib treatment and reveal the molecular basis of differential clinical outcomes with TKI therapy. We find that chromosome 7q gain-induced mTOR signaling activation is associated with poor therapeutic outcomes with Sunitinib treatment, whereas the aristolochic acid signature and VHL mutation synergistically caused enhanced glycolysis is correlated with better prognosis. The proteomic and phosphoproteomic analysis further highlights the responsibility of mTOR signaling for non-response to Sunitinib. Immune landscape characterization reveals diverse tumor microenvironment subsets in ccRCC. Finally, we construct a multi-omics classifier that can detect responder and non-responder patients (receiver operating characteristic–area under the curve, 0.98). Our study highlights associations between ccRCC molecular characteristics and the response to TKI, which can facilitate future improvement of therapeutic responses