Objective:To analyze the relationship of hepatic transit time and portal vein pressure in the patients with portal hypertension and esophagogastric varices, and to clarify its clinical significance.Methods:A total of50hospitalized patients underwent esophagogastric venous embolization due to portal hypertension and esophagogastric varices were selected as observation group, and 50patients without history of liver disease and clinical manifestations of liver disease (hospitalized or out-patient) were selected as control group, All patients underwent liver contrast enhanced ultrasound.The free portal pressure (FPP) was measured by ultrasound guided portal vein puncture for operating pathways in the patients in observation group.The hepatic artery-hepatic vein transit time (HA-HVTT) , the hepatic portal vein-hepatic vein transit time (PV-HVTT) , the liver parenchymahepatic vein transit time (PA-HVTT) of the patients were compared between two groups.The correlations between HA-HVTT, PV-HVTT, PA-HVTT and FPP of the patients in observation group were analyzed.Results:The HA-HVTT, PV-HVTT and PA-HVTT of the patients in observation group were significantly shorter than those in control group (t=5.078, P＜0.01;t=12.163, P＜0.01;t=2.649, P＜0.01) .The HA-HVTT, PV-HVTT and PA-HVTT had negative correlations with FPP in observation group (r=-0.799, P＜0.01;r=-0.554, P＜0.01;r=-0.735, P＜0.01) .The linear relationship between HA-HVTT and FPP was Y=-0.410X+7.254;the linear relationship between PV-HVTT and FPP was Y=-0.355X+4.983;the linear relationship between PA-HVTT and FPP was Y=-0.566X+4.997.Conclusion:Liver transit time can be used as an effective index to judge the portal vein pressure, and it can provide the theroretical basis for the diagnosis and treatment of portal hypertension in the patients.

Purpose: Non-coding RNA activated by DNA damage (NORAD) has been reported to be a cancer-related long non-coding RNA (lncRNA) implicated in the progression of several cancers; however, its role in breast cancer (BC) has not yet been clarified. Methods: Quantitative real-time polymerase chain reaction was used to examine NORAD, microRNA (miR)-155-5p, and suppressor of cytokine signaling 1 (SOCS1) mRNA expression levels. Western blotting was used to analyze SOCS1 protein expression. The malignancy of BC cells was assessed using the cell counting kit-8 (CCK-8), BrdU, and Transwell assays.Bioinformatics analysis, RNA immunoprecipitation assay, and dual-luciferase reporter gene assays were used to verify the targeted relationship between NORAD and miR-155-5p.Additionally, the regulatory effects of NORAD and miR-155-5p on SOCS1 expression were determined by western blotting. Results: NORAD expression was significantly reduced in BC cell lines and tissues, and its low expression was associated with poor tumor tissue differentiation. NORAD overexpression repressed BC cell proliferation, migration, and invasion, whereas its knockdown produced the opposite effects. Additionally, miR-155-5p was found to be a target of NORAD, and the biological functions of miR-155-5p and NORAD were counteractive. MiR-155-5p was confirmed to target SOCS1, and SOCS1 was found to be positively regulated by NORAD. Conclusion NORAD suppresses miR-155-5p to upregulate SOCS1, thereby repressing the proliferation, migration, and invasion of BC cells.

Purpose: Non-coding RNA activated by DNA damage (NORAD) has been reported to be a cancer-related long non-coding RNA (lncRNA) implicated in the progression of several cancers; however, its role in breast cancer (BC) has not yet been clarified. Methods: Quantitative real-time polymerase chain reaction was used to examine NORAD, microRNA (miR)-155-5p, and suppressor of cytokine signaling 1 (SOCS1) mRNA expression levels. Western blotting was used to analyze SOCS1 protein expression. The malignancy of BC cells was assessed using the cell counting kit-8 (CCK-8), BrdU, and Transwell assays.Bioinformatics analysis, RNA immunoprecipitation assay, and dual-luciferase reporter gene assays were used to verify the targeted relationship between NORAD and miR-155-5p.Additionally, the regulatory effects of NORAD and miR-155-5p on SOCS1 expression were determined by western blotting. Results: NORAD expression was significantly reduced in BC cell lines and tissues, and its low expression was associated with poor tumor tissue differentiation. NORAD overexpression repressed BC cell proliferation, migration, and invasion, whereas its knockdown produced the opposite effects. Additionally, miR-155-5p was found to be a target of NORAD, and the biological functions of miR-155-5p and NORAD were counteractive. MiR-155-5p was confirmed to target SOCS1, and SOCS1 was found to be positively regulated by NORAD. Conclusion NORAD suppresses miR-155-5p to upregulate SOCS1, thereby repressing the proliferation, migration, and invasion of BC cells.

ObjectiveThree methods were applied to conduct occupational health risk assessment for the working positions exposed to silicon dusts in a sanitary ceramic manufacturing factory， and the evaluation results were compared to explore the applicability of different occupational health risk assessment methods. MethodsOne large sanitary ceramic product manufacturing enterprise in Songjiang District， Shanghai was selected to conduct occupational health risk assessment for the working positions exposed to silicon dusts， using occupational hazard risk index evaluation method， exposure ratio evaluation method， and International Council on Mining and Metals （ICMM） quantitative occupational health risk assessment method . The consistency of the evaluation results of the three methods was tested using weighted Kappa method. ResultsFourteen working positions exposed to silicon dusts were identified， and three positions had excessive dust concentration： composite forming position of phase 2 workshop （0.80 mg·m^-3）， addition forming position of phase 2 workshop （1.00 mg·m^-3）， and glazing position of 1F in phase 2 workshop （1.50 mg·m^-3）， with an excessive rate of 21.42%. The occupational hazard risk index evaluation method assessed 6 positions with no harm， 6 positions with mild harm， and 2 positions with moderate harm. The ICMM quantitative occupational health risk assessment method assessed 6 positions with potential risks， 2 positions with tolerable risks， and 6 positions with intolerable risks. The exposure ratio evaluation method assessed 8 positions with medium risk， 5 positions with high risk， and 1 position with extremely high risk. The consistency test results of the three evaluation methods were poor. The Kappa coefficient between the occupational hazard risk index evaluation method and the ICMM quantitative occupational health risk assessment method was 0.15. The Kappa coefficient between the occupational hazard risk index evaluation method and the exposure ratio evaluation method was -0.09. The Kappa coefficient between the ICMM quantitative occupational health risk assessment method and the exposure ratio evaluation method was 0.04. The RR values obtained by the three evaluation methods were significantly correlated： the correlation coefficients between RR_{ICMM quantitative assessment method} and RR_{exposure ratio evaluation method}， RR_{Occupational hazard risk index evaluation method} and RR_{ICMM quantitative assessment method}， RR_{Occupational hazard risk index evaluation method} and RR_{exposure ratio evaluation method} were 0.915， 0.604， and 0.594， respectively. The correlation between the assessment result level and C_TWA was strong. ConclusionThe occupational hazard risk index evaluation method is suitable for the working positions with low silicon dust exposure concentration， the ICMM quantitative occupational health risk assessment method and the exposure ratio evaluation method are suitable for the positions with high silicon dust exposure concentration， but all these three evaluation methods have limitations. It is more reasonable to use multiple methods at the same time in actual evaluation work.

OBJECTIVETo investigate the characteristics of the abnormalities of chromosome 17 in myeloid malignancies with complex chromosomal abnormalities (CCAs).

METHODSAbnormalities of chromosome 17 were analyzed in 73 patients with myeloid malignancies with CCAs showed by R banding and conventional karyotyping, including 21 acute myeloid leukemia (AML), 36 chronic myeloid leukemia (CML) and 16 myelodysplastic syndrome (MDS). All CCAs were further analyzed by multiplex fluorescence in situ hybridization (M-FISH).

RESULTSAmong the 73 myeloid malignancies with CCAs, chromosome 17 was the most frequently involved chromosome. It was found in 46.5% (34/73) of all cases, including 12 AML, 13 CML in blast crisis (BC) and 9 MDS. However, it was not found in the 9 CML cases in chronic phase (CP). The majority of changes were structural rearrangements which were identified in 43.8%(32/73)of all cases, among them the frequency was 52.4% (11/21), 33.3% (12/36) and 56.3% (9/16) in AML, CML and MDS, respectively. Numerical abnormalities were detected in 15.1% (11/73) cases, all were monosomy 17, and the frequency was 25.0% (3/12), 38.5% (5/13) and 33.3% (3/9) in AML, CML and MDS, respectively. Both numerical and structural abnormalities of chromosome 17 were found in 9 cases. Unbalanced translocations involving chromosome 17 were much more frequent than balanced ones. In the 3 groups, 16, 15 and 8 unbalanced translocations were found respectively. Only two kind of balanced translocations including t(15;17) in AML and t(15;17;22) in CML were found. All chromosomes were involved except chromosomes 5, 6 and 22 as partner chromosomes, the most common one was chromosome 15 (8.2%), followed by chromosome 2 (5.4%). Five of the 6 cases with translocation of chromosomes 15 and 17 were acute promyelocytic leukemia, the other case was CML-BC.

CONCLUSIONAbnormalities of chromosome 17 were the most frequently involved chromosomal aberrations in myeloid malignancies, and structural rearrangements were more common. All the numerical abnormalities were monosomy 17, unbalanced translocations were much more frequent than balanced ones.

Adolescent ; Adult ; Aged ; Child ; Chromosome Aberrations ; Chromosomes, Human, Pair 17 ; genetics ; Female ; Humans ; In Situ Hybridization, Fluorescence ; Karyotyping ; Leukemia, Myelogenous, Chronic, BCR-ABL Positive ; genetics ; Leukemia, Myeloid, Acute ; genetics ; Male ; Middle Aged ; Myelodysplastic Syndromes ; genetics

Objective To investigate HBV RNA level in patients with HBV-related hepatocellular carcinoma after long-term antiviral therapy and its clinical significance. Methods A total of 60 patients with HBV-related hepatocellular carcinoma who were admitted to Tianjin Second People's Hospital from June 2019 to August 2020 were enrolled in this study. These patients received antiviral therapy with nucleos(t)ide analogues (NAs) for at least two years, and high-sensitivity HBV DNA detection showed a HBV RNA level of < 20 IU/mL at least twice at an interval of 3 months. Liver function, HBV serum markers, and HBV RNA level were measured for all patients. The Kruskal-Wallis H test was used for comparison between multiple groups, and the Wilcoxon rank-sum test was used for comparison between two groups; a Pearson correlation analysis was used to investigate the influencing factors for HBV RNA. Results Among the 60 patients with HBV-related hepatocellualr carcinoma who received long-term antiviral treatment, 9 (15%) tested positive for HBV RNA. According to the level of alpha-fetoprotein (AFP), the patients were divided into AFP positive group and AFP negative group, and there was no significant difference in HBV RNA level between the two groups [0(0-3.57) vs 0(0-2.00), Z =-1.474, P =0.141). According to Barcelona Clinic Liver Cancer (BCLC) stage, they were divided into BCLC stage A group and BCLC stage B+C+D group, and there was no significant difference in HBV RNA level between the two groups [0(0-2.0) vs 0(0-2.0), Z =-0.607, P =0.544]. According to HBeAg level, the patients were divided into HBeAg positive group and HBeAg negative group, and there was a significant difference in HBV RNA level between the two groups [2.99(0-4.80) vs 0(0-0.50), Z =-3.400, P =0.001]. According to the titer of HBsAg, they were divided into HBsAg≤100 IU/mL group, 100 IU/mL < HBsAg < 1500 IU/mL group, and HBsAg ≥1500 IU/mL group, and there was a significant difference in HBV RNA level between the three groups [0(0-0.0) vs 0(0-0.20) vs 2.00(0.0-4.54), H =-7.899, P =0.019]. A Pearson correlation analysis was performed for age, alanine aminotransferase, aspartate aminotransferase, gamma-glutamyl transpeptidase, alkaline phosphatase, alpha-fetoprotein, HBsAg, and HBeAg, and the results showed that HBsAg level was correlated with HBV RNA quantification ( r =0.292, P < 0.05). Conclusion In patients with HBV-related hepatocellualr carcinoma receiving long-term antiviral therapy with NAs, HBV RNA can still be detected after HBV DNA is lower than the lower limit of detection. HBsAg titer may be correlated with serum HBV RNA level.

Due to the low specificity and sensitivity of biomarkers in sepsis diagnostics, the prognosis of sepsis patient outcomes still relies on the assessment of clinical symptoms. Inflammatory response is crucial to sepsis onset and progression; however, the significance of inflammatory response-related genes (IRRGs) in sepsis prognosis is uncertain. This study developed an IRRG-based signature for sepsis prognosis and immunological function. The Gene Expression Omnibus (GEO) database was retrieved for two sepsis microarray datasets, GSE64457 and GSE69528, followed by gene set enrichment analysis (GSEA) comparing sepsis and healthy samples. A predictive signature for IRRGs was created using least absolute shrinkage and selection operator (LASSO). To confirm the efficacy and reliability of the new prognostic signature, Cox regression, Kaplan-Meier (K-M) survival, and receiver operating characteristic (ROC) curve analyses were performed. Subsequently, we employed the GSE95233 dataset to independently validate the prognostic signature. A single-sample GSEA (ssGSEA) was conducted to quantify the immune cell enrichment score and immune-related pathway activity. We found that more gene sets were enriched in the inflammatory response in sepsis patient samples than in healthy patient samples, as determined by GSEA. The signature of nine IRRGs permitted the patients to be classified into two risk categories. Patients in the low-risk group showed significantly better 28-d survival than those in the high-risk group. ROC curve analysis corroborated the predictive capacity of the signature, with the area under the curve (AUC) for 28-d survival reaching 0.866. Meanwhile, the ssGSEA showed that the two risk groups had different immune states. The validation set and external dataset showed that the signature was clinically predictive. In conclusion, a signature consisting of nine IRRGs can be utilized to predict prognosis and influence the immunological status of sepsis patients. Thus, intervention based on these IRRGs may become a therapeutic option in the future.
Humans ; Reproducibility of Results ; Sepsis/genetics* ; Leukocyte Count ; Area Under Curve ; ROC Curve