Search

Background: Evaluation of liver fibrosis played a monumental role in the diagnosis and monitoring of chronic hepatitis B (CHB). We aimed to explore the value of serum N-glycan markers in liver fibrosis. Methods: This multi-center (33 hospitals) study recruited 760 treatment-naïve CHB patients who underwent liver biopsy. Serum N-glycan markers were analyzed by DNA sequencer-assisted fluorophore-assisted with capillary electrophoresis (DSA-FACE) technology. First, we explore the relationship between 12 serum N-glycan markers and the fibrosis stage. Then, we developed a Px score for diagnosing significant fibrosis using the LASSO regression. Next, we compared the diagnostic performances between Px, LSM, APRI, and FIB-4. Finally, we explored the relationships between glycosyltransferase gene and liver fibrosis with RNA-transcriptome sequencing. Results: We included 622 CHB participants: male-dominated (69.6%); median age 42.0 (IQR 34.0–50.0); 287 with normal ALT; 73.0% with significant fibrosis. P5(NA2), P8(NA3), and P10(NA4) were opposite to the degree of fibrosis, while other profiles (except for P0[NGA2]) increased with the degree of fibrosis. Seven profiles (P1[NGA2F], P2[NGA2FB], P3[NG1A2F], P4[NG1A2F], P7[NA2FB], P8[NA3], and P9[NA3Fb]) were selected into Px score. Px score was associated with an increased risk of significant fibrosis (for per Px score increase, the risk of significant fibrosis was increased by 3.54 times (OR = 4.54 [2.63–7.82]) in the fully-adjusted generalized linear model. p for trend was <0.001. The diagnostic performance of the Px score was superior to others. Glycosyltransferase genes were overexpressed in liver fibrosis, and glycosylation and glycosyltransferase-related pathways were significantly enriched. Conclusions: Serum N-glycan markers were positively correlated with liver fibrosis. Px score had good performance in distinguishing significant fibrosis. [ABSTRACT FROM AUTHOR]

BACKGROUND: The correlation between the change in foveal thickness measured using optical coherence tomography (OCT) following surgery for infectious endophthalmitis and preoperative and postoperative visual acuity is uncertain, and there are few pertinent studies on this topic. OBJECTIVE: We explored the variations in macular thickness using OCT after emergency vitrectomy for post-cataract infectious endophthalmitis and the relationship between macular thickness with changes in visual function. METHODS: We included 10 cases of post-cataract infectious endophthalmitis. Each patient underwent 25-G vitrectomy. RESULTS: The infection in all 10 patients was under control and visual function improved. Postoperative vitreous humor culture was positive in 8 patients, including 7 cases of coagulase-negative Staphylococcus epidermidis and 1 case of Lactobacillus acidophilus. The average age of these 10 patients was 71.60 ± 8.71 years (P < 0.05, two-tailed). There was no significant correlation between time 2 (the time of onset after cataract surgery) and visual prognosis. The average time 1 (the time of the vitrification surgery caused by the onset of the disease) was 1.45 ± 0.76 days (P < 0.05, two-tailed). The postoperative 3dVA ranged from 0.20 to 3.00, with an average visual acuity of 1.87 ± 1.12, which was superior to the preoperative value (P < 0.01, two-tailed). The correlation between the post3dVA and post 1mVA was significant. The post 1mVA ranged from 0.05 to 2.20, with an average visual acuity of 0.94 ± 0.74 (P < 0.05, two-tailed). The correlation between post 1mVA and post3mVA was significant. Also, paired t -tests comparing preoperative and postoperative visual acuity revealed a significant correlation (P < 0.05, two-tailed). The post3mVA was 0–1.00 with an average visual acuity of 0.44 ± 0.41. The postoperative foveal thickness ranged from 176.00 to 514.00 μ m, with an average thickness of 281.10 ± 113.12 μ m. CONCLUSION: Emergency 25-G minimally invasive vitrectomy can improve visual acuity and decrease the reoperation rate for patients who have acquired post-cataract infectious endophthalmitis. There were significant correlations between age, disease onset to operation time, preoperative and postoperative visual acuity, and postoperative macular thickness. [ABSTRACT FROM AUTHOR]

Background: Glioma stem‐like cells (GSCs) are greatly responsible for the progression of glioma. Long noncoding RNAs (lncRNAs) play an important role in glioma tumor progression. This study aims to explore the role and underlying mechanism of lncRNA SNHG9 in regulating GSC cell growth. Methods: GSCs were obtained from glioma cells (U87 and U251) and referred to as GSC‐87 and GSC‐251, respectively. The interactions between miR‐326 and SNHG9 or SOX9 were analyzed using luciferase reporter assay. Cell growth of GSCs was evaluated by EdU assay and sphere formation assay. Results: SNHG9 expression was significantly higher in GSC‐87 and GSC‐251 cells than in U87 and U251 cells. SNHG9 overexpression promoted GSC cell growth, whereas SNHG9 knockdown inhibited GSC cell growth. Mechanistically, SNHG9 acted as a competitive endogenous RNA of miR‐326 to elevate the expression of SOX9, a direct target of miR‐326. Moreover, transfection with miR‐326 inhibitor counteracted SNHG9 knockdown‐mediated inhibition of GSC cell growth. Conclusions: SNHG9 facilitates growth of GSCs via the miR‐326/SOX9 axis. This study provides a promising therapeutic target for glioma treatment. [ABSTRACT FROM AUTHOR]