Prognosis of Primary Liver Cancer Based on LI-RADS Classification with Extracellular Agent-Enhanced MRI.

Objective: The prognostic value of the Liver Imaging Reporting and Data System (LI-RADS) 2018 in differentiating hepatocellular carcinoma (HCC) from other primary liver cancers (PLC) with cirrhosis is unclear. We aim to evaluate the value of LI-RADS 2018 with agent-enhanced MRI in the postoperative prognosis of PLC patients with cirrhosis. Methods: Between 2016 and 2021, 432 patients with cirrhosis and surgically proven single primary liver cancer were retrospectively evaluated. Two radiologists evaluated the preoperative MRI features independently and assigned each lesion a LI-RADS category. Overall survival (OS), recurrence-free survival (RFS), and their associated factors were evaluated by using the Kaplan-Meier method, Log rank test, and Cox proportional hazards model. Results: The mean age of 432 patients (239 HCCs, 93 ICCs, and 100 cHCC-CCAs) was 57.27±10.92 years. The LR-M category showed poorer OS and RFS than the LR-4 or LR-5 category did for all primary liver cancers (P <0.001 for both), and so did HCCs with tumor size less than 30mm (P =0.003 and P =0.04, respectively). In the multivariable analysis, the LI-RADS category and tumor size > 30 mm had independent correlations with OS and RFS (all P < 0.05). Multivariable Cox analysis identified rim arterial phase hyperenhancement (APHE) as independent determinants of poor OS and RFS in primary liver cancers (all P < 0.05). Conclusion: The LI-RADS categories can predict the postsurgical prognosis of primary liver cancers independently.

DCE-MRI and DWI can differentiate benign from malignant prostate tumors when serum PSA is ≥10 ng/ml.

Background: This study investigated the diagnostic utility of dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) and diffusion-weighted imaging (DWI) parameters for distinguishing between benign and malignant prostate tumors when serum prostate-specific antigen (PSA) level is ≥10 ng/ml. Methods: Patients with prostate cancer (PCa) and benign prostatic hyperplasia (BPH) with serum PSA ≥10 ng/ml before treatment were recruited. Transrectal ultrasound-guided biopsy or surgery was performed for tumor classification and patients were stratified accordingly into PCa and BPH groups. Patients underwent DCE-MRI and DWI scanning and the transfer constant (Ktrans), rate constant (Kep), fractional volume of the extravascular extracellular space, plasma volume (Vp), and Prostate Imaging Reporting and Data System Version 2 (PI-RADS v2) score were determined. The apparent diffusion coefficient (ADC) was calculated from DWI. The diagnostic performance of these parameters was assessed by receiver operating characteristic (ROC) curve analysis, and those showing a significant difference between the PCa and BPH groups were combined into a multivariate logistic regression model for PCa diagnosis. Spearman's correlation was used to analyze the relationship between Gleason score and imaging parameters. Results: The study enrolled 65 patients including 32 with PCa and 33 with BPH. Ktrans (P=0.006), Kep (P=0.001), and Vp (P=0.009) from DCE-MRI and ADC (P<0.001) from DWI could distinguish between the 2 groups when PSA was ≥10 ng/ml. PI-RADS score (area under the ROC curve [AUC]=0.705), Ktrans (AUC=0.700), Kep (AUC=0.737), Vp (AUC=0.688), and ADC (AUC=0.999) showed high diagnostic performance for discriminating PCa from BPH. A combined model based on PI-RADS score, Ktrans, Kep, Vp, and ADC had a higher AUC (1.000), with a sensitivity of 0.998 and specificity of 0.999. Imaging markers showed no significant correlation with Gleason score in PCa. Conclusion: DCE-MRI and DWI parameters can distinguish between benign and malignant prostate tumors in patients with serum PSA ≥10 ng/ml.

Diagnostic Performance of LI-RADS Version 2018 for Primary Liver Cancer in Patients With Liver Cirrhosis on Enhanced MRI.

Purpose: The study evaluated the diagnostic performance of the Liver Imaging Reporting and Data System (LI-RADS) version 2018 for differentiating hepatocellular carcinoma (HCC) from primary liver cancer in patients with liver cirrhosis based on the updated 2019 WHO classification. Materials and Methods: From 2016 to 2021, 300 patients with surgically confirmed primary liver cancer (PLC) and liver cirrhosis based on the updated 2019 WHO classification were eligible for this retrospective study (100 cases in each of three groups including HCC, ICC, and cHCC-CCA). Two radiologists were blinded to the final diagnosis and independently assigned an LI-RADS category to each liver nodule. The diagnostic performances of the LR-5 category (definitely HCC), and the LR-M category (probably or definitely malignant, but not specific for HCC) were calculated in overall and small observations (<20 mm). Comparisons between groups of categorical variables were performed by one-way analysis of variance and the Chi-squared or Fisher's exact test. Results: The mean age of 300 patients (226 men and 74 women) was 57.40 ± 11.05 years. The sensitivity and specificity of the LR-5 category for differentiating HCCs from other primary liver cancers were 81% (81 of 100) and 82% (164 of 200), respectively. The LR-M category had a sensitivity of 63% (126 of 200) for diagnosing non-HCCs (ICCs and cHCC-CCAs), with a specificity of 90% (90 of 100). The LR-5 category had a sensitivity of 82.5% (33 of 40) for diagnosing HCCs in small observations (<20 mm) with a specificity of 76.6% (59 of 77). On the contrary, LR-M demonstrated slightly higher specificity (93.8%) and sensitivity (73.8%) for diagnosing non-HCCs with tumor size <20 mm. Conclusion: The LR-5 category as well as the LR-M category of Liver Imaging Reporting and Data System (LI-RADS) version 2018 can effectively distinguish hepatocellular carcinoma from other primary hepatic malignancies in patients with liver cirrhosis, especially for small observations (<20 mm).

Exposure to O3 during pregnancy and offspring asthma induced by OVA: Sensitive window identification.

BACKGROUND: Evidence proved that gestational ozone (O3) exposure can increase the risk of neonatal adverse respiratory outcomes, but offspring asthma is unclear. OBJECTIVE: This study aimed to investigate whether gestational O3 exposure could exacerbate offspring asthma, and to research the differences in effects of O3 exposure at different gestational periods on offspring asthma. METHODS: The pregnant ICR mice were randomly grouped and were administered O3 (air as control) at gestational day (GD) 1-6, 7-12, and 13-18, respectively. The pups aged 2-4 weeks were treated with ovalbumin (OVA) to establish a model of early life asthma. Asthma characteristics such as pulmonary inflammation, goblet cell proliferation, airway remodeling, OVA-specific immunoglobulin (Ig) E secretion and cytokines were examined. RESULTS: OVA sensitization and challenge successfully induced asthma in offspring. Compared with the air control, pulmonary inflammation infiltration, mucous secretion, the concentration of OVA-specific IgE, the level of tumor necrosis factor (TNF)-α, and T helper (Th) 2-skewed response were significantly exacerbated when O3 exposure at GD13-18 following inhaling OVA, while pulmonary inflammatory infiltration, mucus secretion, and Th2-skewed response were not significantly changed when O3 exposure at both GD1-6 and GD7-12. What's more, the above indicators in asthmatic offspring due to O3 exposure at GD13-18 were more severe than at GD1-6 and GD7-12. Interestingly, the signs of asthma only appeared in the offspring after OVA inhalation. When offspring were not treated with OVA, the prenatal O3 exposure alone did not lead to asthmatic reactions in offspring. In addition, O3 exposure at GD13-18 markedly increased the number of neutrophils and macrophages in Bronchoalveolar Lavage Fluid (BALF) of asthmatic offspring, and significantly exacerbated Th2 immune imbalance in asthmatic offspring, but had no effect on Th17 immune imbalance. CONCLUSION: Exposure to O3 during pregnancy aggravated asthma in offspring, in which the third trimester is the most sensitive window.

Carbon disulfide induced decidualization disorder in the mice uterus at the window of implantation.

Carbon disulfide (CS2) is regarded as a common occupational poison that is widely used in the textile industry in China. Our previous research suggests that CS2 can induce significant implantation disorders in pregnant mice; however, the specific mechanism remains unclear. Uterine conception in mice must undergo decidualization, which is the prerequisite for propitious blastocyst implantation into the endometrium. Therefore, in this study, we established models of pregnant mice to explore the toxic effects of CS2 on decidualization to elucidate the basic mechanism of implantation disorder after CS2 exposure. The uterine tissues were immediately collected according to the predetermined endpoints to measure the expression levels of IGFBP1 and PRL (markers of decidualization differentiation), IL-11 (representing the secretory function of decidual cells), AKT and pAKT by western blotting, RT-PCR, immunohistochemical staining, H&E staining and ELISA. N-carbamoyl glutamic acid (NCG) acted as an agonist of AKT to verify the upstream regulatory mechanism of decidualization disorder by CS2. The results showed that the normal reaction of decidual transformation was obviously disrupted by CS2 upon 3.5 dpc and 4.5 dpc exposure. The blastocyst did not adhere to the epithelium after 3.5 dpc-exposure and did not invade the endometrium after 4.5 dpc-exposure, resulting in its suspension in the uterine cavity, stagnation and eventual loss. The proteins expression levels were decreased by 95.2% for IGFBP1 and 76.2% for PRL at the 4.5 dpc endpoint after 3.5 dpc CS2 exposure compared with the control. Simultaneously, the mRNA and protein expression levels of IL-11 in uterine tissues were significantly reduced by CS2, and consistent decreasing trends over time were observed for IGFBP1 and PRL, compared with the control. Additionally, the ratio of pAKT/AKT protein expression was decreased by 72.2% and 94.8% at 12 h and 18 h after 3.5 dpc exposure and by 53.3% and 74.3% at 6 h and 12 h after 4.5 dpc exposure, respectively, compared with the corresponding controls. Furthermore, NCG could recover the IGFBP1 and PRL protein expression, which was increased by 27.5% and 52.3% at 4.5 dpc and 6.5 dpc, respectively, after 3.5 dpc exposure for IGFBP1 and by 30.3% at 6.5 dpc after 4.5 dpc exposure for PRL, compared with CS2 exposure alone. Collectively, this study suggested that the decidualization disorder caused by CS2 at the window of implantation in pregnant mice, which is triggered by pAKT, contributed to the implantation disorder and eventually led to embryo loss. It is worth noting that our study may provide a new perspective and reference for exploring the toxic mechanism of implantation disorder and even infertility in harmful circumstances.

Prenatal O3 exposure increases the severity of OVA-induced asthma in offspring.

BACKGROUND: Accumulating epidemiological studies showed that prenatal and early life exposure to ambient air pollution was important contributor to the development of childhood asthma. However, the effects and mechanisms of prenatal exposure to ozone (O3), a type of ambient air pollution, on the progression of asthma in offspring remain unclear. OBJECTIVE: This study aimed to determine the effects and mechanism of asthma in offspring after prenatal O3 exposure. METHODS: Pregnant BALB/c mice were exposed to O3 or air on gestational days (GDs) 13-18. Their offspring were sensitized and challenged to ovalbumin (OVA) to establish asthma model, and the asthma features were evaluated. The splenic natural killer (NK) cells in the offspring were measured to explore the mechanism on the effects of asthma in the offspring. The responses of the pregnant mice and dams after O3 exposure were evaluated. RESULTS: Airway inflammation, mucus secretion, OVA-specific immunoglobulin (Ig) E, T helper (Th) 2-skewed response, the frequency of CD3ε-CD49b+ splenic NK cells, the expression of tumor necrosis factor (TNF)-α, and IL (interleukin)-17 were significantly exacerbated in the OVA-induced asthma offspring after prenatal O3 exposure. In addition, airway inflammation, a lower number of CD3ε-CD49b+ splenic NK cells, and systemic oxidative stress were caused at the end of pregnancy after O3 exposure, which did not recover at the end of lactation for the first two responses. CONCLUSIONS: Prenatal O3 exposure increased the severity of OVA-induced asthma in the offspring, which might be directly induced by CD3ε-CD49b+ splenic NK cells in the offspring and indirectly related to the damaged maternal immune system.

Modelling the biological performance of a side-stream membrane bioreactor using ASM1.

Membrane bioreactors (MBRs) are attracting global interest but the mathematical modeling of the biological performance of MBRs remains very limited. This study focuses on the modelling of a side-stream MBR system using Activated Sludge Model No. 1 (ASM1), and comparing the results with the modelling of traditional activated sludge processes. ASM1 parameters relevant for the long-term biological behaviour in MBR systems were calibrated (i.e. Y(H) = 0.72gCOD/gCOD, Y(A) = 0.25gCOD/gN, b(H) = 0.25 d(-1), b(A) = 0.080 d(-1) and f(P) = 0.06), and generally agreed with the parameters in traditional activated sludge processes, with the exception that a higher autotrophic biomass decay rate was observed in the MBR. A sensitivity analysis for steady state operation and DO dynamics suggested that the biological performance of the MBR system (the sludge concentration, effluent quality and the DO dynamics) are very sensitive to the parameters(i.e. Y(H), Y(A), b(H), b(A), micro(maxH) and micro(maxA)), and influent wastewater components(X(I), S(S), X(S), S(NH)).