Risk factors for and predictive nomogram of overall survival in adult patients with craniopharyngiomas: A SEER population-based study.

Studies with relatively large sample size as well as long-term follow-up focusing on adult craniopharyngioma (CP) patients are still lacking. We attempted to identify independent prognostic factors and establish a nomogram model to estimate survival rates for adult CP patients. The Surveillance, Epidemiology, and End Results database was used to obtain data on patients with CP. Univariable and multivariable Cox analyses were utilized to identify the prognostic factors of adult CP patients. A survival prediction model was constructed and its predictive performance was also assessed. A total of 991 patients (695 in training group and 296 in validation group) were eligible for final inclusion. Multivariate Cox analysis presented that age at diagnosis, marital status, race, tumor size, and surgery type were statistically significant prognostic factors for overall survival (all P < .05). A graphical predicting nomogram model was developed to calculate the predicted patients' survival probabilities at 1, 2, 5, and 10 years. The concordance indexes were 0.708 ± 0.019 and 0.750 ± 0.025 for the training and validation samples, respectively, demonstrating favorable discrimination abilities. Similarly, the time-dependent area under curve also showed overall satisfactory discrimination ability. Favorable consistencies between the predicted and actual survival were presented according to the calibration curves. An easy-to-use nomogram, being proven to be with reliable discrimination ability and accuracy, was established to help predict overall survival for adult patients with CP using the identified significant prognostic factors.

Alleviation of sepsis-associated encephalopathy by ginsenoside via inhibition of oxidative stress and cell apoptosis: An experimental study.

Ginsenoside (Rg1) has biological effects including anti-oxidation, anti-inflammation, neuroprotection and neural function improvement, but with few studies in sepsis-associated encephalopathy (SAE). This study thus evaluated Ginsenoside in alleviating SAE, suppressing oxidative stress (OS) or neuronal apoptosis. SAE mouse model was generated and were assigned into SAE, SAE + LD-Rg1, and SAE + HD-Rg1 groups to measure neural apoptosis by flow cytometry. Contents of malondialdehyde (MDA), superoxide dismutase (SOD), GSH-Px and caspase-3 were quantified, and mouse neural reflex function was evaluated. Expression of Nrf2, HO-1 was measured. Mouse neuron MN-c and microglia BV2 were co-cultured in control, LPS, LPS+Rg1 (20µM) and LPS+Rg1 (40µM) groups. Iba-1 expression of BV2 cells was measured by flow cytometry. Contents of tumor necrosis factor-α (TNF-α), interleukin-1ß (IL-1ß), and IL-6 were quantified. Apoptosis of MN-c cells was measured by flow cytometry, and reactive oxygen species (ROS) content was measured by DCFH-DA staining. SAE mice had elevated caspase-3 activity, cell apoptosis, MDA content, and decreased SOD, GSH-Px activity or neural reflex score comparing to Sham group. Rg1 treatment suppressed caspase-3 activity, apoptotic rate or MDA content, recovered SOD activity, neural reflex score, and expression of Nrf2 and HO-1. LPS treatment elevated Iba-1 expression and release of inflammatory cytokines TNF-α, IL-1ß and IL-6, induced MN-c apoptosis or ROS production, and enhanced Nrf2 and HO-1 expression. Rg1 treatment remarkably inhibited LPS-induced response or cell apoptosis. Ginsenoside can alleviate SAE damage via up-regulating Nrf2 and HO-1 to enhance anti-OS potency and to reduce neural cell apoptosis.

Circulating long noncoding RNA ZNFX1 antisense RNA negatively correlates with disease risk, severity, inflammatory markers, and predicts poor prognosis in sepsis patients.

This study aimed to investigate the correlation of long noncoding RNA (lncRNA) ZNFX1 antisense RNA (ZFAS1) with disease risk, severity, inflammation markers, and prognosis in sepsis patients.A total of 202 sepsis patients were consecutively enrolled, and 200 healthy volunteers were also recruited as healthy controls (HCs). Plasma samples of all patients and HCs were collected. LncRNA ZFAS1 expression was determined by quantitative polymerase chain reaction assay and inflammatory cytokines levels were detected by enzyme-linked immunosorbent assay.The median value of lncRNA ZFAS1 expression in sepsis patients was (0.639 [0.325-1.071]), which was lower compared to HCs (1.957 [0.876-3.245], P < .001], and receiver operating characteristics (ROC) curve revealed that lncRNA ZFAS1 expression had a good diagnostic value for sepsis with area under curve (AUC) of 0.814 (95% confidence interval [CI]: 0.771-0.857). Spearman test disclosed that lncRNA ZFAS1 expression was negatively correlated with Acute Physiology and Chronic Health Evaluation (APACHE) II score (r = -0.505, P < .001), and it was negatively associated with levels of C-creative protein (r = -0.241, P = .001), tumor necrosis factor-α (r = -0.253, P < .001), and interleukin (IL)-6 (r = -0.177, P = .012) while positively associated with IL-10 level (r = 0.173, P = .014). Also, lncRNA ZFAS1 expression was lower in survivor group compared to nonsurvivor group (P < .001), and it presented with a good predictive value on distinguishing nonsurvivors from survivors in sepsis patients with AUC of 0.628 (95% CI: 0.538-0.717).Circulating lncRNA ZFAS1 expression negatively correlates with disease risk, severity, and inflammatory markers levels, and might predict worse survival in sepsis patients.

Circulating lncRNA IFNG-AS1 expression correlates with increased disease risk, higher disease severity and elevated inflammation in patients with coronary artery disease.

BACKGROUND: This study aimed to investigate the associations of circulating long, non-coding (lncRNA) IFNG-AS1, lncRNA ANRIL and lncRNA ITSN1 relative expressions with disease risk, severity and inflammatory cytokines levels in coronary artery disease (CAD) patients. METHODS: One hundred and ninety-one patients suspected of CAD who underwent coronary angiography were consecutively enrolled in this casecontrol study, and divided into CAD patients (N = 102) and controls (N = 89) according to coronary angiographic results. Blood samples of all participants were collected. Plasma lncRNA IFNG-AS1, lncRNA ANRIL and lncRNA ITSN1 expressions were detected using quantitative polymerase chain reaction (qPCR). Serum tumor necrosis factor-α (TNF-α), interleukin (IL)-1ß (IL-1ß), IL-6, IL-8, IL-10, and IL-17 were assessed using enzyme-linked immunosorbent assay (ELISA). Gensini Score was used to evaluate the disease severity of CAD patients. RESULTS: LncRNA IFNG-AS1 relative expression in CAD patients was upregulated compared with that in controls (P < .001), and the receiver operating characteristic (ROC) curve showed that the area under curve (AUC) of lncRNA-IFNG-AS1 for predicting the risk of CAD was 0.755 (95% CI: 0.688-0.821). lncRNA IFNG-AS1 relative expression was remarkably associated with Gensini Score (r = .259, P = .009). Additionally, lncRNA IFNG-AS1 relative expression was positively associated with high-sensitivity C-reactive protein (hs-CRP) (r = .283, P = .004), TNF-α (r = .269, P = .006), and IL-6 levels (r = .425, P < .001), while it was negatively correlated with IL-10 level (r = -.263, P = .008). lncRNA ANRIL or lncRNA ITSN1 was not correlated with CA D risk, Gensini Score, hs-CRP, ESR, TNF-α, IL-1ß, IL-6, IL-8, IL-10, or IL-17 levels (all P > .05). CONCLUSION: Circulating lncRNA IFNG-AS1 expression correlates with increased disease risk, higher disease severity and elevated inflammation in CAD patients.