Geriatric Nutritional Risk Index and the Survival of Patients with Hepatocellular Carcinoma: A Meta-Analysis.

Malnutrition is a risk factor of adverse clinical outcome in patients with cancer. Recent studies suggest that geriatric nutritional risk index (GNRI) could reflect the nutritional status in patients with various clinical conditions. The aim of the systematic review and meta-analysis was to evaluate the association between GNRI and survival of patients with hepatocellular carcinoma (HCC). Observational studies evaluating the association between pretreatment GNRI and survival of patients with HCC were obtained by search of PubMed, Web of Science, Embase, Wanfang, and CNKI databases. A random-effects model was used to pool the results after incorporating the potential influence of heterogeneity. Seven cohort studies including 2636 patients with HCC contributed to the meta-analysis. Pooled results showed that HCC patients with low pretreatment GNRI were associated with poor overall survival [hazard ratio (HR): 1.77, 95% confidence interval (CI): 1.32 to 2.37, p<0.001; I2=66%) and progression-free survival (HR: 1.62, 95% CI: 1.39 to 1.89, p<0.001; I2=0%) as compared to those with normal GNRI. Sensitivity analyses by excluding one study at a time showed similar results (p all<0.05). Subgroup analyses showed that the association between low pretreatment GNRI and poor survival of patients with HCC was not significantly affected by age of the patients, main treatment, cutoff of GNRI, or the follow-up durations. In conclusion, malnutrition indicated by a low pretreatment GNRI may be a risk factor of poor survival of patients with HCC.

LncRNA ATP1A1-AS1 inhibits cell proliferation and promotes cell apoptosis in thyroid carcinoma by regulating the miR-620/IRF2BP2 axis.

BACKGROUND: Thyroid carcinoma (THCA) is a common malignancy of the endocrine system. Further understanding of the molecular mechanism underlying THCA is crucial to develop effective diagnostic therapy and improve its treatments. In this study, we intended to provide novel direction for THCA targeted therapy from the aspect of lncRNA-miRNA-mRNA interaction. We aimed to investigate the function and molecular mechanism of lncRNA ATP1A1-AS1 in THCA. METHODS: Gene expression was assessed by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Cell growth was detected by CCK-8 and EdU assays. Flow cytometry was applied for analyzing cell apoptosis. The binding of ATP1A1-AS1 or IRF2BP2 to miR-620 was validated by RNA pulldown and luciferase reporter assays. The protein levels were examined by western blotting. RESULTS: ATP1A1-AS1 was decreased in THCA cells and tissues. ATP1A1-AS1 overexpression attenuated cell growth and promoted apoptosis. MiR-620, which was upregulated in THCA, was identified as a direct target of ATP1A1-AS1. Furthermore, IRF2BP2 was discovered to be a target of miR-620, which displayed low expression in THCA cells and tissues. Importantly, IRF2BP2 knockdown reversed the influence of ATP1A1-AS1 overexpression on THCA cell proliferation and apoptosis. CONCLUSIONS: LncRNA ATP1A1-AS1 inhibited cell growth and promotes apoptosis in THCA via the miR-620/IRF2BP2 axis.

IncRNA TYMSOS Promotes Epithelial-Mesenchymal Transition and Metastasis in Thyroid Carcinoma through Regulating MARCKSL1 and Activating the PI3K/Akt Signaling Pathway.

Thyroid carcinoma (THCA) has been increasing in incidence greater than other cancers. Long noncoding RNAs (lncRNAs) were reported to play crucial roles in THCA development. Our study aimed to explore the underlying mechanism of lncRNA thymidylate synthetase opposite strand RNA (TYMSOS) in THCA. TYMSOS and myristoylated alanine rich protein kinase C substrate like 1 (MARCKSL1) were upregulated whereas miR-130a-5p was downregulated in THCA cells and tissues. The results of loss-of-function assays showed that TYMSOS knockdown inhibited cell metastasis and epithelial-mesenchymal transition (EMT) in THCA. TYMSOS was primarily distributed in the cytoplasm of THCA cells, as shown by FISH assay. RNA pulldown and luciferase reporter assay further showed that TYMSOS binds with miR-130a-5p. Luciferase reporter assay also revealed that MARCKSL1 is targeted by miR-130a-5p. Rescue assay showed that the suppression of TYMSOS downregulation on THCA cell malignant behaviors was reversed by MARCKSL1 overexpression. Additionally, overexpressing MARCKSL1 offset the inhibition of TYMSOS downregu-lation on the PI3K/Akt signaling pathway. TYMSOS knockdown inhibits the growth of THCA tumors, as in vivo assays showed. Collectively, TYMSOS facilitates THCA progression by sponging miR-130a-5p and upregulating MARCKSL1 to activate the PI3K/Akt signaling pathway, providing new avenues for THCA treatment.

Dietary xylo-oligosaccharide ameliorates colonic mucus microbiota penetration with restored autophagy in interleukin-10 gene-deficient mice.

BACKGROUND: Inflammatory bowel disease (IBD) is, nowadays, highly prevalent and presents a global clinical challenge. The objective of this study is to assess the effects of xylo-oligosaccharide (XOS) on Il10-/- mice, a classic animal model of IBD. METHODS: Male wild-type (WT) mice were assigned to WT group, and Il10-/- mice were assigned to interleukin-10 gene-deficient (IL-10-KO) group and XOS group, respectively. There were 6-8 mice aged 8 weeks in each group. Mice in the XOS group received 1.0 g/kg/day XOS by gavage for 4 weeks. RESULTS: Compared with mice in IL-10-KO group, Il10-/- mice with XOS intervention presented significant mild spontaneous colitis with lower disease activity index, histological scores, and bowel inflammatory cytokine levels. Dietary XOS downregulated bowel mucus bacterial penetration, which occurred as early as the onset of bowel colitis. The effect of XOS was associated with restored expression of LC3II/I and decreased expression of p62 and beclin-1 in colon. CONCLUSIONS: Therefore, XOS decreases colonic mucus microbiota penetration with restored function of antophagy. Our findings suggest that XOS may be a potential dietary supplement or functional food for early management of IBD.

Photoperiod-responsive changes in chromatin accessibility in phloem companion and epidermis cells of Arabidopsis leaves.

Photoperiod plays a key role in controlling the phase transition from vegetative to reproductive growth in flowering plants. Leaves are the major organs perceiving day-length signals, but how specific leaf cell types respond to photoperiod remains unknown. We integrated photoperiod-responsive chromatin accessibility and transcriptome data in leaf epidermis and vascular companion cells of Arabidopsis thaliana by combining isolation of nuclei tagged in specific cell/tissue types with assay for transposase-accessible chromatin using sequencing and RNA-sequencing. Despite a large overlap, vasculature and epidermis cells responded differently. Long-day predominantly induced accessible chromatin regions (ACRs); in the vasculature, more ACRs were induced and these were located at more distal gene regions, compared with the epidermis. Vascular ACRs induced by long days were highly enriched in binding sites for flowering-related transcription factors. Among the highly ranked genes (based on chromatin and expression signatures in the vasculature), we identified TREHALOSE-PHOSPHATASE/SYNTHASE 9 (TPS9) as a flowering activator, as shown by the late flowering phenotypes of T-DNA insertion mutants and transgenic lines with phloem-specific knockdown of TPS9. Our cell-type-specific analysis sheds light on how the long-day photoperiod stimulus impacts chromatin accessibility in a tissue-specific manner to regulate plant development.

[Three-dimensional chromosome conformation capture and its derived technologies].

Linear chromatin is compacted into eukaryotic nucleus through a complex and multi-layered architecture. Consequently, chromatin conformation in a local or long-distance manner is strongly correlated with gene expression. Chromosome conformation capture (3C) technology, together with its variants like 4C/5C/Hi-C, has been well developed to study chromatin looping and whole genome structure. In this review, we introduce new technologies including chromosome capture combined with immunoprecipitation, nuclei acid-based hybridization, single cell and genome sequencing, as well as their application.

Improvement of Laser Transmission Welding of Glass with Titanium Alloy by Laser Surface Treatment.

Laser surface treatment of the titanium alloy was locally oxidized on the metal surface to improve the joint strength of laser transmission welding of high borosilicate glass with titanium alloy. The results find that the welding strength was increased 5 times. The welding mechanism was investigated by the morphology of the welded parts, the tensile-fracture failure mode, the diffusion of the interface elements, and the surface free energy. The results show that there are many adherents between the titanium alloy and high borosilicate glass after tensile fracture, the welding strength was higher when the laser voltage was 460 V, and the tensile⁻fracture failure mode is mainly ductile fracture. Element-line scanning analysis revealed that elemental diffusion occurred in the two materials, which is an important reason for the high welding strength. Surface free-energy analysis shows that laser surface treatment improves the surface free energy of titanium alloy, promotes the wettability and compatibility, and increases the welding strength of titanium alloy with glass.