Prevalence of and risk factors for non-suicidal self-injury in rural China: Results from a nationwide survey in China

Background Non-suicidal self-injury (NSSI) is a highly prevalent and serious public health problem among adolescents worldwide. However, to date there were no studies assessing the prevalence of NSSI defined by suggested DSM-5 criteria among Chinese adolescents. We aimed to conduct a nationwide survey to explore the prevalence of and risk factors for NSSI among school-based adolescents in rural China. Methods A total sample of 15,623 adolescents in rural China were enrolled by using a multistage sampling method. Data was collected by self-report questionnaires including demographic characteristics, neglect, maltreatment, loneliness, resilience, social support and emotional management ability. NSSI was defined by suggested DSM-5 criteria, according to which the engagement in self-injury took place more than 5 times a year. Multinomial logistic regression models were used to estimate the association between risk factors and NSSI. Results There were 12.2% of adolescents (n = 1908) met the suggested DSM-5 criteria. Approximately 29% reported a history of NSSI at least once during the last year. Significant differences were found in several demographic factors including gender, ethnicity, grade, and family structure between adolescents with and without experiencing NSSI. The top three NSSI behaviors among adolescents with NSSI experience were hitting self, pinching, and pulling hair, with a prevalence rate of 16.7%, 14.1% and 11.2%, respectively. Female, Han ethnicity, fathers’ education level, neglect, maltreatment, loneliness, social support, suicidal behaviors and emotional management ability were significantly associated with NSSI by multivariate analysis. No significant relationship was found between resilience and risk of NSSI. Limitation The DSM-5 has proposed 6 groups of criteria for NSSI, we only used criteria on frequency given its more accepted feasibility and pragmatic application. Consequently, it may different from other prevalence that estimated by other criteria. Conclusion To the best of our knowledge, this is the first study reporting prevalence of NSSI defined by suggested DSM-5 criteria among adolescent in rural China. In comparison to finding from the similar samples of adolescents, Chinese rural adolescents seem to have a relative higher prevalence. The potential risk factors for NSSI include female, father's education, Han ethnicity, psychosocial factors and suicide behaviors. More evidence for further understanding of context of the occurrence, improving access to health care utilization, and identifying the role of psychosocial factors and family relationship, is needed for the prevention and management of NSSI.Published versio

Detection of the Diffuse Supernova Neutrino Background with JUNO

As an underground multi-purpose neutrino detector with 20 kton liquid scintillator, Jiangmen Underground Neutrino Observatory (JUNO) is competitive with and complementary to the water-Cherenkov detectors on the search for the diffuse supernova neutrino background (DSNB). Typical supernova models predict 2-4 events per year within the optimal observation window in the JUNO detector. The dominant background is from the neutral-current (NC) interaction of atmospheric neutrinos with 12C nuclei, which surpasses the DSNB by more than one order of magnitude. We evaluated the systematic uncertainty of NC background from the spread of a variety of data-driven models and further developed a method to determine NC background within 15\% with {\it{in}} {\it{situ}} measurements after ten years of running. Besides, the NC-like backgrounds can be effectively suppressed by the intrinsic pulse-shape discrimination (PSD) capabilities of liquid scintillators. In this talk, I will present in detail the improvements on NC background uncertainty evaluation, PSD discriminator development, and finally, the potential of DSNB sensitivity in JUNO

Recovery of Residual Carbon from Ti-Extraction Blast Furnace Slag by Flotation with Simultaneous Dechlorination

Ti-extraction blast furnace slag (EBFS) is a secondary slag produced by titanium extraction of titanium-bearing blast furnace slag (TBBFS), which is challenging to be used directly because of its residual carbon and chlorine. This study was performed to recover the residual carbon and remove chlorine from EBFS by froth flotation. The finely ground EBFS (FEBFS) contained graphitized carbon and khamrabaevite and had a 10.19% loss on ignition (LOI) and 5.52% Cl. The graphitized carbon was mainly recovered by flotation rather than khamrabaevite. Graphitized carbon appeared as flakes embedded in or stacked on the surface of the concentrate grains. The irregular-shaped particles were amorphous aluminosilicate glasses, whose presence adversely affected the quality and performance of the flotation concentrate. The Cl contents of the flotation concentrate and tailings obtained under the optimized flotation conditions were significantly reduced to 1.17% and 0.4%, respectively. The dechlorination efficiency reached 71.56%. Meanwhile, the LOI of flotation tailing was reduced to 1.32% and the carbon recovery was 84.79%. Froth flotation could recover residual carbon and remove chlorine from EBFS simultaneously, a novel way to deal with EBFS as a resource and harmless process

Herpes Simplex Virus 1 Tegument Protein UL46 Inhibits TANK-Binding Kinase 1-Mediated Signaling

HSV-1 has evolved multiple strategies to evade host antiviral responses and establish a lifelong latent infection, but the molecular mechanisms by which HSV-1 interrupts antiviral innate immunity are not completely understood. As TBK1 is very critical for antiviral innate immunity, it is of great interest to reveal the immune evasion mechanism of HSV-1 by targeting TBK1. In the present study, HSV-1 UL46 was found to inhibit the activation of IFN-I by targeting TBK1, suggesting that the evasion of TBK1 mediated antiviral innate immunity by HSV-1 UL46. Findings in this study will provide new insights into the host-virus interaction and help develop new approaches against HSV-1 infection.TANK-binding kinase 1 (TBK1) is a key component of the antiviral immunity signaling pathway. It activates downstream interferon regulatory factor 3 (IRF3) and subsequent type I interferon (IFN-I) production. Herpes simplex virus type 1 (HSV-1) can antagonize host antiviral immune responses and lead to latent infection. Here, HSV-1 tegument protein UL46 was demonstrated to downregulate TBK1-dependent antiviral innate immunity. UL46 interacted with TBK1 and reduced TBK1 activation and its downstream signaling. Our results showed that UL46 impaired the interaction of TBK1 and IRF3 and downregulated the activation of IRF3 by inhibiting the dimerization of TBK1 to reduce the IFN-I production induced by TBK1 and immunostimulatory DNA. The IFN-I and its downstream antiviral genes induced by UL46-deficient HSV-1 (ΔUL46 HSV-1) were higher than those of wild-type HSV-1 (WT HSV-1). In addition, the stable knockdown of TBK1 facilitated the replication of ΔUL46 HSV-1, but not WT HSV-1. Together, these findings reveal a novel mechanism of immune evasion by HSV-1

SMYD3 induces sorafenib resistance by activating SMAD2/3-mediated epithelial-mesenchymal transition in hepatocellular carcinoma

Summary: Drug resistance prominently hampers the effects of systemic therapy of sorafenib to hepatocellular carcinoma (HCC). Epigenetics have critical regulatory roles in drug resistance. However, the contributions of histone methylatransferase SET and MYND domain containing 3 (SMYD3) to sorafenib resistance in HCC remain largely unknown. Here, using our established sorafenib-resistant HCC cell and xenograft models, we found SMYD3 was markedly elevated in sorafenib-resistant tumors and cells. Functionally, loss- and gain-of-function studies showed that SMYD3 promoted the migration, invasion, metastasis and stemness of sorafenib-resistant HCC cells. Mechanistically, SMYD3 is required for SMAD2/3-mediated epithelial-mesenchymal transition (EMT) in sorafenib-resistant HCC cells by interacting with SMAD2/3 and epigenetically promoting the expression of SOX4, ZEB1, SNAIL1 and MMP9 genes. In summary, our data demonstrate that targeting SMYD3 is an effective approach to overcome sorafenib resistance in HCC

Biological Control and Plant Growth Promotion by Volatile Organic Compounds of Trichoderma koningiopsis T-51

Trichoderma spp. are widely used in plant disease control and growth promotion due to their high efficacy and multiple biocontrol mechanisms. Trichoderma koningiopsis T-51 is an effective biocontrol agent against gray mold disease by direct contact. However, the indirect physical contact biocontrol potential of Trichoderma spp. is not clear. In this study, the volatile organic compounds (VOCs) produced by T-51 showed high inhibitory activity against plant pathogenic fungi Botrytis cinerea and Fusarium oxysporum. The percentage of B. cinerea and F. oxysporum mycelial growth inhibition by T-51 VOCs was 73.78% and 43.68%, respectively. In both B. cinerea and F. oxysporum, conidial germination was delayed, and germ tube elongation was suppressed when exposed to T-51 VOCs, and the final conidial germination rate of B. cinerea decreased significantly after T-51 treatment. The VOCs from T-51 reduced the Botrytis fruit rot of tomato compared with that noted when using the control. Moreover, the T-51 VOCs significantly increased the size and weight of Arabidopsis thaliana seedlings. Twenty-four possible compounds, which were identified as alkenes, alkanes, and esters, were detected in VOCs of T-51. These results indicate that T. koningiopsis T-51 can exert biological control by integrating actions to suppress plant disease and promote plant growth

Hepatitis B virus X protein promotes interleukin-7 receptor expression via NF-κB and Notch1 pathway to facilitate proliferation and migration of hepatitis B virus-related hepatoma cells

Abstract Background Interleukin-7 receptor (IL-7R) is involved in the abnormal function of solid tumors, but the role and regulatory mechanisms of IL-7R in HBV-related hepatocellular carcinoma (HCC) are still unclear. Methods Gene and protein expression levels of IL-7R were examined in hepatoma cells transfected with hepatitis B virus (HBV) plasmids and in hepatoma cells transfected with the multifunctional nonstructural protein X (HBX). The expression of HBX and IL-7R was measured by immunohistochemical analysis in HBV-related HCC tissues. The role of NF-κB and Notch1 pathways in HBX-mediated expression of IL-7R in hepatoma cells was examined. Activation of IL-7R downstream of intracellular signaling proteins AKT, JNK, STAT5, and the associated molecules CyclinD1 and matrix metalloproteinase-9 (MMP)-9, was assessed in HBX-positive cells with or without treatment with IL-7R short hairpin RNA (shRNA). Additionally, the role of IL-7R in HBX-mediated proliferation and migration of hepatoma cells was investigated. Results The expression of IL-7R was increased in hepatoma cells transfected with HBV plasmids; HBX was responsible for the HBV-mediated upregulation of IL-7R. Compared to adjacent tissues, the expression of HBX and IL-7R was increased in HBV-related HCC tissues. Additionally, the relative expression levels of HBX were associated with IL-7R in HBV-related HCC tissues. The activation of NF-κB pathways and expression of Notch1 were increased in hepatoma cells transfected with HBX, and inhibition of NF-κB and Notch1 pathways significantly decreased HBX-mediated expression of IL-7R. The activation of AKT and JNK and the expression of CyclinD1 and MMP-9 were increased in HBX-positive cells. When cells were treated with IL-7R shRNA, the activation of AKT and JNK, as well as the expression of CyclinD1 and MMP-9, were significantly inhibited. Additionally, IL-7R was responsible for HBX-induced proliferation and migration ability of hepatoma cells. Conclusions Our data demonstrate that HBX can upregulate IL-7R via NF-κB and Notch1 pathways to facilitate the activation of intracellular pathways and expression of associated molecules, and contribute to proliferation and migration of hepatoma cells