Significant changes in soil microbial community structure and metabolic function after Mikania micrantha invasion.

Currently, Mikania micrantha (M. micrantha) has invaded Guangdong, Guangxi and other provinces in China, causing serious harm to the forests of southeastern China. Soil microorganisms play an important role in the establishment of M. micrantha invasion, affecting plant productivity, community dynamics, and ecosystem function. However, at present, how M. micrantha invasion affects soil carbon, nitrogen, and phosphorus phase functional genes and the environmental factors that cause gene expression changes remain unclear, especially in subtropical forest ecosystems. This study was conducted in Xiangtoushan National Forest Park in Guangdong Province to compare the changes in soil nutrients and microorganisms after M. micrantha invasion of a forest. The microbial community composition and metabolic function were explored by metagenome sequencing. Our results showed that after M. micrantha invasion, the soil was more suitable for the growth of gram-positive bacteria (Gemmatimonadetes). In addition, the soil microbial community structure and enzyme activity increased significantly after M. micrantha invasion. Correlation analysis and Mantel test results suggested that total phosphorus (TP), nitrate nitrogen (NO3--N), and soil dissolved organic matter (DOM; DOC and DON), were the strong correlates of soil microbial nitrogen functional genes, while soil organic matter (SOM), soil organic carbon (SOC), total nitrogen (TN), and available phosphorus (Soil-AP) were strongly correlated with the expression of soil microbial phosphorus functional gene. Mikania micrantha invasion alters soil nutrients, microbial community composition and metabolic function in subtropical forests, creates a more favorable growth environment, and may form a positive feedback process conducive to M. micrantha invasion.

Corrigendum to "Dual Effects of Cellular Immunotherapy in Inhibition of Virus Replication and Prolongation of Survival in HCV-Positive Hepatocellular Carcinoma Patients".

[This corrects the article DOI: 10.1155/2016/6837241.].

DESIGN AND DEVELOPMENT OF HUMAN COMPUTER INTERFACE USING ELECTROOCULOGRAM WITH DEEP LEARNING.

Today's life assistive devices were playing significant role in our life to communicate with others. In that modality Human Computer Interface (HCI) based Electrooculogram (EOG) playing vital part. By using this method we can able to overcome the conventional methods in terms of performance and accuracy. To overcome such problem we analyze the EOG signal from twenty subjects to design nine states EOG based HCI using five electrodes system to measure the horizontal and vertical eye movements. Signals were preprocessed to remove the artifacts and extract the valuable information from collected data by using band power and Hilbert Huang Transform (HHT) and trained with Pattern Recognition Neural Network (PRNN) to classify the tasks. The classification results of 92.17% and 91.85% were shown for band power and HHT features using PRNN architecture. Recognition accuracy was analyzed in offline to identify the possibilities of designing HCI. We compare the two feature extraction techniques with PRNN to analyze the best method for classifying the tasks and recognizing single trail tasks to design the HCI. Our experimental result confirms that for classifying as well as recognizing accuracy of the collected signals using band power with PRNN shows better accuracy compared to other network used in this study. We compared the male subjects performance with female subjects to identify the performance. Finally we compared the male as well as female subjects in age group wise to identify the performance of the system. From that we concluded that male performance was appreciable compared with female subjects as well as age group between 26 to 32 performance and recognizing accuracy were high compared with other age groups used in this study.

Mangiferin Attenuated Diethynitrosamine-Induced Hepatocellular Carcinoma in Sprague-Dawley Rats via Alteration of Oxidative Stress and Apoptotic Pathway.

Liver cancer is the fifth commonly occurring cancer worldwide with the annual death rate of 9.1%. Hepatocellular carcinoma is the most frequent kind of primary liver cancer and occurs mostly in patients with chronic liver disease and cirrhosis. Because the cancer is generally detected only in the later stages, it is often treated with therapies such as radiation, ablation, and chemotherapy, which produces serious side effects and has a low recovery rate. Therefore, researchers are now focused on herbal-based drugs with increased efficacy and with no side effects to treat cancer. One such drug is mangiferin, a xanthanoid possessing augmented antioxidant, anti-inflammatory, and antidiabetic properties. The present study investigated the anticarcinogenic property of mangiferin against DEN-induced hepatocellular carcinoma. Hepatocellular carcinoma was induced in healthy Sprague-Dawley rats by treating them with 0.01% diethylnitrosamine (DEN) in the drinking water for 12 weeks, followed by 50 mg of mangiferin for a period of 8 weeks. Biochemical, oxidative stress markers, antioxidant status, and tumor marker level in the DEN- and DEN + mangiferin-treated rats liver were assessed to detect the efficacy of mangiferin in inhibiting cancer induction. The anticarcinogenic property of mangiferin was confirmed by evaluating the apoptotic protein expression and histological analysis of liver tissue from DEN- and DEN + mangiferin-treated rats. Our results show that mangiferin possesess anticarcinogenic properties against DEN-induced hepatocellular carcinoma. We predict that further investigation will reveal mangiferin as a potent drug to treat liver cancer.

Factors associated with optimal pain management in advanced cancer patients.

PURPOSE: To analyze clinical factors that were associated with inadequate pain control in cancer patients with metastatic malignancy and moderate to severe baseline pain. PATIENTS: We retrospectively analyzed data from 260 advanced cancer patients who admitted to the First Hospital of Jilin University (Jilin, China) from January 2012-May 2013. MEASUREMENTS: Statistical analysis was performed to assess the correlation between pain control and baseline characteristics including, gender, patient age, type of malignancy, presence of bone metastases, pain intensity, pain location, etiology of pain, type of pain, and presence of breakthrough pain. MAIN RESULTS: A total of 75.4% of patients obtained satisfactory pain control (numerical rating scale ≤ 3) in 3 days. Baseline characteristics including gastrointestinal tumors (P = 0.032), severe pain (P < 0.001), and frequent breakthrough pain (P < 0.001) were independent risk factors of poor pain control in the 3-day treatment. These factors were also significantly associated with longer time needed to achieve stable pain control. Of the 185 patients treated with opioids, higher doses of analgesics were used in younger patients (<60 years old; P = 0.018), and in patients with severe pain (P < 0.001), neuropathic pain (P = 0.002), and frequent breakthrough pain (P = 0.015). CONCLUSIONS: Factors associated with more difficult pain control include gastrointestinal tumor, severe baseline pain, presence of breakthrough pain, and neuropathic etiology of pain.

Up-regulation of FGF15/19 signaling promotes hepatocellular carcinoma in the background of fatty liver.

BACKGROUND: Upregulated fibroblast growth factor 19 (FGF19) expression in human hepatocellular carcinoma (HCC) specimens is associated with tumor progression and poor prognosis. Nonalcoholic steatohepatitis (NASH) patients are at high risk for malignant transformation into HCC. METHODS: A steatohepatitis-HCC model was established in male C57L/J mice treated with N-nitrosodiethylamine (DEN) and high-fat diet (HFD). A mouse HCC cell line (Hepa1-6) and a mouse hepatocyte line (FL83B) were used to elucidate the mechanism by free fatty acids (FFA) treatment. FGF15, the mouse orthologue of FGF19, and it receptor fibroblast growth factor receptor4 (FGFR4) as well as co-receptor ß-klotho were studied. FGF19 signaling was also studied in human samples of HCC with steatohepatitis. RESULTS: HCC incidence and tumor volume were significantly increased in the DEN+HFD group compared to that in the DEN+control diet (CD) group. Increased levels of FGF15/FGFR4/ß-klotho, aberrant epithelial-mesenchymal transition (EMT) and Wnt/ß-catenin signaling were detected in DEN+HFD mice. Blockage of the FGF15 signal can attenuate cell migration ability and aberrant EMT and Wnt/ß-catenin signaling. CONCLUSIONS: Up-regulated FGF15/FGFR4 signaling promoted the development of HCC by activation of EMT and Wnt/ß-catenin signaling in the lipid metabolic disorder microenvironment. Further investigation of FGF19/FGFR4 signaling is important for potential early diagnosis and therapeutic targeting in HCC patients.

Lentivirus­mediated MDA7/IL24 expression inhibits the proliferation of hepatocellular carcinoma cells.

MDA7/IL24 is a member of the IL­10 gene family that functions as a cytokine. Notably, supra­physiological endogenous MDA7 levels have been indicated to suppress tumor growth and induce apoptosis in different cancer types. In the present study, MDA7 roles were investigated during the proliferation of hepatocellular carcinoma (HCC) cells and the molecular mechanisms underlying this process. A lentiviral vector expressing MDA7/IL24 (LV­MDA7/IL24) was constructed and used to infect HCC SMMC­7721 cells. The expression levels of MDA7/IL24 in these cells were determined using RT­qPCR and western blot analysis. The effects of LV­MDA7/IL24 on cell proliferation were analyzed using MTT and colony formation assays. Furthermore, the influence of LV­MDA7/IL24 on cell apoptosis and cell cycle distribution were detected using flow cytometry. The underlying molecular mechanisms were investigated using microarray and western blot analysis. The expression of MDA7/IL24 was confirmed to be significantly increased in the cells infected with LV­MDA7/IL24 compared with that the negative­control infected group. Lentivirus­mediated MDA7/IL24 expression was found to inhibit HCC cell proliferation and colony formation, and it also induced cell arrest and apoptosis. Microarray analysis and western blotting results indicated that multiple cancer­associated pathways and oncogenes are regulated by MDA7/IL24, including cell cycle regulatory and apoptosis activation pathway. In conclusion, it was determined that MDA7/IL24 inhibits the proliferation and reduces the tumorigenicity of HCC cells by regulating cell cycle progression and inducing apoptosis, indicating that it may be used as a potential prognostic and therapeutic target in HCC.

The Mitogen-Activated Protein Kinase Kinase VdPbs2 of Verticillium dahliae Regulates Microsclerotia Formation, Stress Response, and Plant Infection.

Verticillium dahliae, a ubiquitous phytopathogenic fungus, forms resting structures, known as microsclerotia that play crucial roles in Verticillium wilt diseases. VdHog1, a mitogen-activated protein kinase (MAPK), controls microsclerotia formation, virulence, and stress response in V. dahliae. In this study, we present detailed evidence that the conserved upstream component of VdHog1, VdPbs2, is a key regulator of microsclerotia formation, oxidative stress and fungicide response and plant virulence in V. dahliae. We identified VdPbs2, homologous to the yeast MAPK kinase Pbs2. Similar to the VdHog1 deletion mutant, VdPbs2 deletion strains exhibited delayed melanin synthesis and reduced formation of microsclerotia. When exposed to stresses, VdPbs2 mutants were more sensitive than the wild type to osmotic agents and peroxide, but more resistant to inhibitors of cell wall synthesis and some fungicides. Finally, VdPbs2 deletion mutants exhibited reduced virulence on smoke tree and tobacco seedlings. When taken together, we implicate that VdPbs2 and VdHog1 function in a cascade that regulates microsclerotia formation and virulence, but not all VdHog1 dependent functions are VdPbs2 regulated. This study thus provides novel insights into the signal transduction mechanisms that regulate microsclerotia formation and pathogenesis in this fungus.

Dual Effects of Cellular Immunotherapy in Inhibition of Virus Replication and Prolongation of Survival in HCV-Positive Hepatocellular Carcinoma Patients.

Immune cells play an important role in the development and progression of hepatitis C virus (HCV) and hepatocellular carcinoma (HCC). We conducted a retrospective study to evaluate the influence of adoptive cellular immunotherapy (CIT) on viral load and progression-free survival (PFS) for HCC patients infected with HCV. Patients (n = 104) were divided into a control group (conventional therapy, n = 73) and study group (combination of CIT and conventional therapy, n = 31). Autologous mononuclear cells were induced into natural killer, γδT, and cytokine-induced killer cells and infused intravenously to study group patients. More patients had shown viral load decrease or were stable in study group (100% versus 75%) (p = 0.014). The median PFS of the study group and control group was 16 and 10 months, respectively (p = 0.0041), and only CIT was an independent prognostic factor for PFS (hazard ratio, 0.422; p = 0.005). Three patients developed transient moderate fever after infusion, and there were no significant differences in alanine aminotransferase and aspartate aminotransferase levels before and after treatment in both groups. Our results show that CIT contributes to improvement of prognosis and inhibition of viral replication in HCV-related HCC patients, without impairment of liver function.

Prognostic value of serum AFP, AFP-L3, and GP73 in monitoring short-term treatment response and recurrence of hepatocellular carcinoma after radiofrequency ablation.

PURPOSE: Alpha-fetoprotein (AFP), Lens culinaris agglutinin-reactive fraction of AFP (AFP-L3), and Golgi protein 73 (GP73) levels have been widely used as tumor markers for the diagnosis of hepatocellular carcinoma (HCC). The aim of this study was to investigate whether these tumor markers could be used to monitor short-term treatment response and recurrence of HCC in patients undergoing radiofrequency ablation (RFA). METHODS: Between July 2012 and July 2013, 53 consecutive patients with newly diagnosed HCC were prospectively enrolled in this study. Among these, 32 patients underwent RFA, after which they were followed up prospectively at the First Hospital of Jilin University in China. RESULTS: AFP, AFP-L3, and GP-73 values pre-RFA were not associated with tumor size, whereas AFP and GP-73 levels tended to be associated with tumor number, the presence of vascular invasion, deterioration of liver function, advanced-stage disease, and a poor performance status. GP-73 levels were dramatically elevated in the patients with hepatitis C-associated HCC. Neither pre-RFA nor 1-month post-RFA tumor marker values were associated with short-term outcome. The short-term recurrence rate of AFP-positive patients measured 1 month post-RFA was obviously higher than that of AFP-negative patients. CONCLUSIONS: AFP and GP-73 values were associated with clinical variables representing tumor growth and invasiveness, and the AFP value measured 1 month post-RFA was a strong predictor of short-term recurrence in patients with HCC.

Combination of radiofrequency ablation and sequential cellular immunotherapy improves progression-free survival for patients with hepatocellular carcinoma.

Hepatocellular carcinoma (HCC) recurs frequently after minimally invasive therapy. The aim of our study was to observe the efficiency and safety of the combined treatment of radiofrequency ablation (RFA) with cellular immunotherapy (CIT) for HCC patients. In our study, 62 patients with HCC who were treated with radical RFA were divided into two groups: RFA alone (32 patients) and RFA/CIT (30 patients). Autologous mononuclear cells were collected from the peripheral blood and separated by apheresis, and then induced into natural killer (NK) cells, γδT cells and cytokine-induced killer (CIK) cells. These cells were identified by flow cytometry with their specific antibodies and then were infused intravenously to RFA/CIT patients for three or six courses. The tumor recurrent status of these patients was evaluated with computed tomography or magnetic resonance imaging every 3 months after RFA. Progression-free survival (PFS), liver function, viral load and adverse effects were examined. The results implied that PFS was higher in RFA/CIT group than that in RFA group. In RFA/CIT group, six courses had better survival prognosis than three courses. Viral load of hepatitis C was decreased in two of three patients without antiviral therapy in RFA/CIT group, but was increased in RFA group. No significant adverse reaction was found in the patients with CIT. In summary, these preliminary results suggest that combination of sequential CIT with RFA for HCC patients was efficient and safe, and may be helpful in the prevention of the recurrence for the patients with HCC after RFA.