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Identification of snoRNA SNORA71A as a Novel Biomarker in Prognosis of Hepatocellular Carcinoma
Background. Small nucleolar RNAs (snoRNAs) have been proved to play important roles in various cellular physiological process. Recently, dysregulation of snoRNA SNORA71A has been found involved in tumorigenesis of various malignant cancers. However, the emerging effects of SNORA71A in hepatocellular carcinoma (HCC) remain largely unclear. In this study, we aimed to explore the SNORA71A expression and its underlying significance in HCC. Methods. Expression of SNORA71A in cell lines and clinical specimens was measured by quantitative real-time PCR. Then, all enrolled HCC patients were divided into low and high SNORA71A expression subgroups and then they were compared in the aspects of clinical features as well as survival outcome by respective statistical analysis methods. Results. SNORA71A was significantly downexpressed in SK-HEP-1 (), Huh-7 (), Hep3B (), and clinical HCC specimens (). Comparing the clinical features between SNORA71A expression subgroups, it showed that low SNORA71A expression was significantly associated with large tumor diameter, multiple lesions, capsular invasion, bad tumor differentiation, and TNM stage (). Furthermore, it was found that HCC patients with lower SNORA71A expression had higher risk in postoperative tumor relapse (median time: 9.5 vs. 35.2 months; low vs. high; ) and poor overall survival (median time: 36.8 vs. 52.9 months; low vs. high; ). Besides, SNORA71A expression served as independent risk factors for tumor-free (; 95% CI [0.263-0.770]; ) and long-term survival (; 95% CI [0.127-0.657]; ). Conclusions. Our study for the first time demonstrated that downregulation of SNORA71A could serve as a novel biomarker for clinical assessment and prognostic prediction of HCC patients.
Usefulness of Cathepsin S to Predict Risk for Obstructive Sleep Apnea among Patients with Type 2 Diabetes
Background. Obstructive sleep apnea (OSA) was highly prevalent in patients with type 2 diabetes (T2D). Cathepsin S (CTSS), a cysteine protease, is involved in the inflammatory activity in T2D and hypoxia conditions. The aim of the study was to evaluate whether CTSS could be involved in the inflammatory reaction of OSA in patients with T2D. Methods. We included 158 participants in this study matched for age, gender, and body mass index in 4 groups (control, non-OSA&T2D, OSA&non-T2D, and OSA&T2D). After overnight polysomnography, we collected the clinical data including anthropometrical characteristics, blood pressure, and fasting blood samples in the morning. Plasma CTSS concentration was evaluated using the human Magnetic Luminex Assay. Results. Compared with the control group, both the non-OSA&T2D group and the OSA&non-T2D group showed higher CTSS levels. Plasma CTSS expression was significantly increased in subjects with OSA&T2D compared to subjects with non-OSA&T2D. The OSA&T2D group had higher CTSS levels than the OSA&non-T2D group, but there were no statistically significant differences. Plasma CTSS levels showed significant correlation with the apnea-hypopnea index (AHI) (, ) and plasma fasting blood glucose (, ). After adjusting confounding factors, plasma CTSS levels were independently associated with the AHI (Beta: 0.386, 95% confidence intervals (CI): 21.988 to 57.781; ). Furthermore, we confirmed the higher pinpoint accuracy of plasma CTSS in the diagnosis of OSA (area under the curve: 0.868). Conclusions. Plasma CTSS expression was significantly elevated in the OSA&T2D group and was independently associated with the AHI; it could be a biomarker with a positive diagnostic value on diagnosing OSA among patients with T2D.
Cardiopulmonary Bypass Induces Acute Lung Injury via the High-Mobility Group Box 1/Toll-Like Receptor 4 Pathway
During cardiopulmonary bypass (CPB), pulmonary ischemia/reperfusion (I/R) injury can cause acute lung injury (ALI). Our previous research confirmed that abnormal high-mobility group box 1 (HMGB1) release after CPB was closely related to ALI. However, the mechanism underlying the HMGB1-mediated induction of ALI after CPB is unclear. Our previous study found that HMGB1 binds Toll-like receptor 4 (TLR4), leading to lung injury, but direct evidence of a role for these proteins in the mechanism of CPB-induced lung injury has not been shown. We examined the effects of inhibiting HMGB1 or reducing TLR4 expression on CPB-induced lung injury in rats administered anti-HMBG1 antibody or TLR4 short-hairpin RNA (shTLR4), respectively. In these rat lungs, we studied the histologic changes and levels of interleukin- (IL-) 1β, tumour necrosis factor- (TNF-) α, HMGB1, and TLR4 after CPB. After CPB, the lung tissues from untreated rats showed histologic features of injury and significantly elevated levels of IL-1β, TNF-α, HMGB1, and TLR4. Treatment with anti-HMGB1 attenuated the CPB-induced morphological inflammatory response and protein levels of IL-1β, TNF-α, HMGB1, and TLR4 in the lung tissues and eventually alleviated the ALI after CPB. Treatment with shTLR4 attenuated the CPB-induced morphological inflammatory response and protein levels of IL-1β, TNF-α, and TLR4 in the lung tissues and eventually alleviated the ALI after CPB, but could not alleviate the HMGB1 protein levels induced by CPB. In summary, the present study demonstrated that the HMGB1/TLR4 pathway mediated the development of ALI induced by CPB.
PD-L1 Expression Level Displays a Positive Correlation with Immune Response in Pancreatic Cancer
The expression of PD-L1 could be a novel biomarker which predicts that patients are more likely to respond to immunotherapy. Our study investigated the relationship among clinicopathological characteristics, prognosis, PD-L1 expression levels, and FOXP3+ Treg infiltration. In addition, the relationship among clinicopathological characteristics, prognosis, PD-L1 expression levels, and FOXP3+ Treg infiltration was explored. Furthermore, the relationship between PD-L1 expression and FOXP3+ Treg infiltration was examined. We found that 41.3% of pancreatic cancer patients had PD-L1-positive staining; both PD-L1 expression levels and FOXP3+ Treg infiltration were significantly associated with depth of invasion, lymph node metastasis, distant metastasis, and pTNM. In addition, PD-L1 expression and FOXP3+ Treg infiltration also could be prognostic biomarkers for pancreatic cancer.
Relationship between Plasma Lipoprotein-Associated Phospholipase A2 Concentrations and Apolipoprotein in Stable Coronary Artery Disease Patients
Background. Increasing evidence states that the plasma lipoprotein-associated phospholipase A2 (Lp-PLA2) levels and apolipoprotein particles are regarded as the risk maker for cardiovascular heart disease. Nevertheless, the issue about whether Lp-PLA2 is associated with apolipoprotein particles in individuals who have been diagnosed as stable coronary artery disease (CAD) remains largely unexplored. Method. All 569 participants engaged in this research, who never took lipid-lowering drugs, had been divided into groups by the coronary angiography (CAG), namely, stable CAD: ; non-CAD: . The results concerning Lp-PLA2 levels were calculated by Elisa Kit, while apolipoprotein particles were measured by the department of laboratory. Results. The plasma concentration of Lp-PLA2 was remarkably higher in stable CAD group than the non-CAD group ( vs. , ). Pearson correlation analyses explained the plasma Lp-PLA2 concentration was correlated with apoB (, ) and apoB/apoA1 (, ), not associated with apoA1 (, ). Conversely, the association remains unobserved among non-CAD patients except apoA1. Moreover, multiple linear regression revealed the relations between Lp-PLA2 concentrations and apoB (, ), as well as apoB/apoA1 (, ), but not apoA1 (, ). After adjustment for several risk factors regarding CAD, like hypertension, gender, smoking, age, and diabetes mellitus, there had still been positive associations between the Lp-PLA2 concentration and apoB (, ), as well as apoB/apoA1 (, ). Conclusion. The plasma levels of Lp-PLA2 provide positively a key link with apoB, apoB/apoA-1 among stable CAD, denoting the communication between Lp-PLA2 and apolipoprotein particles in the state of CAD.
Evaluation of Altered Glutamatergic Activity in a Piglet Model of Hypoxic-Ischemic Brain Damage Using 1H-MRS
Background and Objective. The excitotoxicity of glutamate (Glu) is a major risk factor for neonatal hypoxic-ischemic brain damage (HIBD). The role of excitatory amino acid transporter 2 (EAAT2) and the α-amino-3-hydroxy-5-methyl-4-isoxazole-proprionic acid receptor (AMPAR) subunit GluR2 in mediating the Glu excitotoxicity has always been the hotspot. This study was aimed at investigating the early changes of glutamate metabolism in the basal ganglia following hypoxia-ischemia (HI) in a neonatal piglet model using 1H-MRS. Methods. Twenty-five newborn piglets were selected and then randomly assigned to the control group () and the model group () subjected to HI. HI was induced by blocking bilateral carotid blood flow under simultaneous inhalation of a 6% oxygen mixture. 1H-MRS data were acquired from the basal ganglia at the following time points after HI: 6, 12, 24, and 72 h. Changes in protein levels of EAAT2 and GluR2 were determined by immunohistochemical analysis. Correlations among metabolite concentrations, metabolite ratios, and the protein levels of EAAT2 and GluR2 were investigated. Results. The Glu level sharply increased after HI, reached a transient low level of depletion that approached the normal level in the control group, and subsequently increased again. Negative correlations were found between concentrations of Glu and EAAT2 protein levels (, ) and between the Glu/creatine (Cr) ratio and EAAT2 protein level (, ). Moreover, changes in GluR2 protein level were significantly and negatively correlated with those in Glu level (the absolute Glu concentration, , ; Glu/Cr, , ). Conclusions. Changes in Glu level measured by 1H-MRS were inversely correlated with those in EAAT2 and GluR2 protein levels following HI, and the results demonstrated that 1H-MRS can reflect the early changes of glutamatergic activity in vivo.