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BACKGROUND The objective of this study was to investigate the relationship between engagement in multiple risk behaviours (MRB) and concussion amongst youth. METHODS This was a cross-sectional study that used survey data collected from 3059 students in grades 6-10 (approximate ages 11-15 years) from Ontario, Canada. Students reported whether or not they had a medically diagnosed concussion within the previous 12 months and the frequency that they participated in several risky behaviours including fighting, bullying, smoking, drinking alcohol, using illicit drugs, drinking caffeinated beverages, not using protective equipment, and having unsafe sex. Responses to the risky behavior items were used to create a MRB score. The association between MRB and concussion was explored using logistic regression that controlled for several confounding variables. RESULTS Approximately 10.7% of students reported that they had a medically diagnosed concussion within the past year. selleck chemical A dose-response relationship was found between MRB and concussion among students in grades 9-10, while in grades 6-8 students only those in the highest MRB quartile had an increased likelihood of concussion. The relative odds for concussion in the highest versus the lowest MRB quartile were 4.67 (95% confidence interval 2.33, 9.35) in grades 9-10 students and 2.94 (95% confidence interval, 1.90, 4.56) in grades 6-8 students. CONCLUSIONS Engagement in MRB may be an important etiologic component of adolescent concussion. Future studies should address whether behavioural interventions designed to decrease engagement in MRB reduce the risk of concussion and other injuries.BACKGROUND The reconstruction of large head and face missing structures in the craniofacial region in children is very challenging for plastic surgeons. Expanded local and expanded axial-pattern flaps are widely used for the reconstruction of large-area scars. Free flaps are used very cautiously in children. 3D printing technology is a new technology with great development potential. 3D printing technology is used to assist in individualizing titanium alloy restorations for prefabricated skull defect repair. This application has great advantages in the repair of large skull loss. However, it is crucial to choose appropriate techniques and treat deformities of the head and face with integrated approaches and collaboration among multiple departments. CASE PRESENTATION This study proposes a method to combine the expanded flap method and 3D printing technology to achieve natural remodeling of the craniofacial region in a child. CONCLUSION Large area of head and face missing structures can be reconstructed by using expanded skin flaps combined with 3D printing, and patients can get better new faces.BACKGROUND Retinoblastoma (RB) is the most common intraocular malignancy in children. Long non-coding RNA X-inactive specific transcript (lncRNA XIST) has been reported to be associated with RB, but research on the mechanism of XIST is not well studied. METHODS Expressions of XIST, microRNA-140-5p (miR-140-5p), and sex-determining region Y-related high-mobility group box 4 (SOX4) were analyzed by qRT-PCR or Western blot. Relationships of XIST, SOX4, and miR-140-5p were evaluated by dual-luciferase reporter assay and Spearman's analysis. Cell Counting Kit-8 (CCK-8) and Transwell assay were performed to assess the function of XIST on RB cell proliferation and invasion. RESULTS In RB tissues, XIST and SOX4 expressions were obviously increased, but the miR-140-5p expression was markedly reduced. XIST expression was positively related to SOX4 expression while negatively correlated with miR-140-5p expression, and negative correlation was exhibited between miR-140-5p and SOX4 expression in RB tissues. XIST was confirmed to directly bind to miR-140-5p, and SOX4 was one target of miR-140-5p. XIST knockdown could impede RB cell proliferation and invasion, while miR-140-5p inhibition reversed the effects. In addition, XIST overexpression or miR-140-5p inhibition could abrogate the inhibition of SOX4 silencing on cell proliferation and invasion of RB cells. CONCLUSIONS XIST was obviously increased in RB tissues and cells, and XIST inhibition repressed the proliferation and invasion of RB cells by miR-140-5p/SOX4 axis, which may provide new understandings of the XIST molecular mechanism in RB.BACKGROUND The use of monoclonal antibodies in various settings has been linked to the development of progressive multifocal leukoencephalopathy (PML). link2 Whilst this association is well-described with agents such as rituximab and natalizumab, the literature describing the occurrence of PML with ofatumumab therapy (especially in a haematology setting) is sparse. This case aims to draw attention to the above association with a particular focus on the mechanisms by which B-cell-depleting therapy can precipitate PML during the treatment of haematological malignancy. CASE PRESENTATION A 68-year-old Caucasian man presented with acute-on-subacute confusion and reduced mobility. He had a history of chronic lymphocytic leukaemia for which he had completed six cycles of ofatumumab and chlorambucil 2 months prior to presentation. Biochemistry, physical examination and imaging were unremarkable on admission. Subsequent neurological examination demonstrated diminished reflexes and an extensor right plantar, while magnetic rreatment of PML.The promising expectations about personalized medicine have opened the path to routine large-scale sequencing and increased the importance of genetic counseling for hereditary cancers, among which hereditary breast and ovary cancers (HBOC) have a major impact. High-throughput sequencing, or Next-Generation Sequencing (NGS), has improved cancer patient management, ameliorating diagnosis and treatment decisions. In addition to its undeniable clinical utility, NGS is also unveiling a large number of variants that we are still not able to clearly define and classify, the variants of uncertain significance (VUS), which account for about 40% of total variants. At present, VUS use in the clinical context is challenging. Medical reports may omit this kind of data and, even when included, they limit the clinical utility of genetic information. This has prompted the scientific community to seek easily applicable tests to accurately classify VUS and increase the amount of usable information from NGS data. In this review, we will focus on NGS and classification systems for VUS investigation, with particular attention on HBOC-related genes and in vitro functional tests developed for ameliorating and accelerating variant classification in cancer.BACKGROUND Tick-borne encephalitis virus (TBEV) is a member of the Flaviviridae family, Flavivirus genus, which includes several important human pathogens. It is responsible for neurological symptoms that may cause permanent disability or death, and, from a medical point of view, is the major arbovirus in Central/Northern Europe and North-Eastern Asia. TBEV tropism is critical for neuropathogenesis, yet little is known about the molecular mechanisms that govern the susceptibility of human brain cells to the virus. In this study, we sought to establish and characterize a new in vitro model of TBEV infection in the human brain and to decipher cell type-specific innate immunity and its relation to TBEV tropism and neuropathogenesis. METHOD Human neuronal/glial cells were differentiated from neural progenitor cells and infected with the TBEV-Hypr strain. Kinetics of infection, cellular tropism, and cellular responses, including innate immune responses, were characterized by measuring viral genome and viral titer,immunity is likely to contribute to shaping TBEV tropism for human brain cells. They describe a new in vitro model for in-depth study of TBEV-induced neuropathogenesis and improve our understanding of the mechanisms by which neurotropic viruses target and damage human brain cells.The recent advent of third-generation sequencing technologies brings promise for better characterization of genomic structural variants by virtue of having longer reads. However, long-read applications are still constrained by their high sequencing error rates and low sequencing throughput. Here, we present NanoVar, an optimized structural variant caller utilizing low-depth (8X) whole-genome sequencing data generated by Oxford Nanopore Technologies. NanoVar exhibits higher structural variant calling accuracy when benchmarked against current tools using low-depth simulated datasets. In patient samples, we successfully validate structural variants characterized by NanoVar and uncover normal alternative sequences or alleles which are present in healthy individuals.BACKGROUND Chitinase 3 like 1 protein (Chi3L1) is expressed in several cancers, and a few evidences suggest that the secreted Chi3L1 contributes to tumor development. However, the molecular mechanisms of intracellular Chi3L1 are unknown in the lung tumor development. METHODS In the present study, we generated Chi3L1 knockout mice (Chi3L1KO(-/-)) using CRISPR/Cas9 system to investigate the role of Chi3L1 on lung tumorigenesis. link3 RESULTS We established lung metastasis induced by i.v. injections of B16F10 in Chi3L1KO(-/-). The lung tumor nodules were significantly reduced in Chi3L1KO(-/-) and protein levels of p53, p21, BAX, and cleaved-caspase 3 were significantly increased in Chi3L1KO(-/-), while protein levels of cyclin E1, CDK2, and phsphorylation of STAT3 were decreased in Chi3L1KO(-/-). Allograft mice inoculated with B16F10 also suppressed tumor growth and increased p53 and its target proteins including p21 and BAX. In addition, knockdown of Chi3L1 in lung cancer cells inhibited lung cancer cell growth and upregulated p53 expression with p21 and BAX, and a decrease in phosphorylation of STAT3. Furthermore, we found that intracellular Chi3L1 physically interacted and colocalized with p53 to inhibit its protein stability and transcriptional activity for target genes related with cell cycle arrest and apoptosis. In lung tumor patient, we clinically found that Chi3L1 expression was upregulated with a decrease in p53 expression, as well as we validated that intracellular Chi3L1 was colocalized, reversely expressed, and physically interacted with p53, which results in suppression of the expression and function of p53 in lung tumor patient. CONCLUSIONS Our studies suggest that intracellular Chi3L1 plays a critical role in the lung tumorigenesis by regulating its novel target protein, p53 in both an in vitro and in vivo system.BACKGROUND Inflammation and oxidative stress induced by oxidized low density lipoprotein are the main causes of vascular endothelial injury and atherosclerosis. Endothelial cells are important for the formation and repair of blood vessels. However, the detailed mechanism underlying the regulation of maturity and antioxidation of stem cell-derived endothelial like cells remains unclear. Besides, YY1 and TET2 play a key role on epigenetic modifications of proliferation and differentiation of stem cells. However, the regulatory mechanism of epigenetic modification induced by YY1 and TET2 on stem cells to iECICs is also not clear. AIM Here, we want to investigate detailed mechanism underlying the regulation of maturity and antioxidation of stem cell-derived iECICs by by YY1 and TET2. METHODS The qPCR, Western blot, immunohistochemical staining and flow cytometric analysis were used to analyze the expression level of each gene. Luciferase reporter assay was used to detect the binding sites between microRNA and target genes.