Differences in clinical characteristics and liver injury between patients diagnosed with the Omicron subvariant BA.5.2 and the prototype of SARS-CoV-2: a single center retrospective study.

BACKGROUND: The purpose of this study was to investigate the differences between the clinical characteristics and the factors influencing liver injury in patients with the Omicron subvariant BA.5.2 (Omicron BA.5.2) and the prototype of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). METHODS: Between December 30, 2019 and November 30, 2022, 157 patients infected with the SARS-CoV-2 prototype and 199 patients infected with the Omicron BA.5.2 were included in this case-control, single-center, retrospective study. Differences in clinical characteristics and liver injury between the Omicron BA.5.2 patients and the prototype patients were subsequently analyzed. RESULTS: None of the Omicron BA.5.2 patients reached the critical state, and showed relatively milder symptoms including fever, cough, headache, muscle soreness, nausea or vomiting, diarrhea, anorexia and hypoxia. The Omicron BA.5.2 had a lower effect on body temperature (T), white blood cell (WBC) count, hematocrit (HCT), C-reactive protein (CRP) level, D-dimer, finger pulse oxygen saturation (SpO2) and lung lesions. The differences in liver injury between the two groups were related to the severity of the disease, T, blood oxygen levels, albumin (ALB), CRP, and medication usage. Gender, body mass index, and CRP levels influenced liver damage in the Omicron BA.5.2 patients. In particular, CRP was an independent risk factor for liver injury. Because the severity of liver function damage was considerably low, only a small number of Omicron BA.5.2 patients required liver-protective treatment. CONCLUSION: Liver injury is expected in the COVID-19 patients. The Omicron BA.5.2 patients showed milder symptoms of liver injury than the prototype patients. However, dynamic monitoring of liver function is warranted, especially for individuals presenting with elevated levels of CRP.

The long non-coding RNA UPAT promotes gastric cancer cell progression via UHRF1.

BACKGROUND: LncRNA ubiquitin-like with PHD and RING finger domains 1 (UHRF1) protein associated transcript (UPAT) regulates the progression of many cancers. However, its role in gastric cancer (GC) is less frequently reported. OBJECTIVE: In the context of the promoting effect of lncRNA on modulating GC progression, detailed insights into the role and underlying mechanism of UPAT in GC are the foothold in this study. METHODS: Overall survival was calculated. The mRNA expressions of UPAT and UHRF1 were measured by qRT-PCR, and the protein expressions of UHRF1, Cyclin D1 and cleaved caspase-3 were determined by western blot. Cell viability, growth, migration and invasion were assessed by CCK-8, colony formation, wound healing and Transwell assays, respectively. Apoptosis rate and cell cycle were assayed by flow cytometry. RESULTS: UPAT was overexpressed in GC tissue and cell lines. Decreased UPAT level was associated with higher overall survival. Down-regulation of UPAT diminished cell proliferation, Cyclin D1 expression, and migration and invasion rates, increased apoptosis rate and cleaved caspase-3 expression, and blocked cell cycle in AGS and NCI-N87 cells. UPAT expression in GC was positively correlated with UHRF1 expression. UHRF1 overexpression offset the inhibitory effects of UPAT down-regulation on cell proliferation, migration, invasion and cell cycle, and partially reversed the positive effect of UPAT down-regulation on apoptosis. CONCLUSION: UPAT might positively regulate the progression of GC via interacting with UHRF1. The UHRF1/UPAT axis revealed in the present study may provide a promising approach to intervene in the progression of GC.

Differences in clinical characteristics and liver injury between suspected and confirmed COVID-19 patients in Jingzhou, Hubei Province of China.

ABSTRACT: To evaluate the clinical characteristics and liver injury in coronavirus disease 2019 (COVID-19) patients, and analyze the differences between suspected and confirmed COVID-19 patients, this retrospective study was performed on 157 COVID-19 patients and 93 suspected patients who were ultimately excluded from COVID-19 (control patients). Differences in clinical characteristics and liver injury between suspected and confirmed COVID-19 patients were analyzed. Age, male sex, fever, chest tightness and dyspnea were related to the severity of COVID-19. C-reactive protein (CRP) and D-dimer may be predictors of the severity of COVID-19. Computed tomography (CT) played an important role in the screening of COVID-19 and the evaluation of disease severity. Multiple factors may cause liver injury in COVID-19 patients. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) may be more likely to cause liver injury than common respiratory infectious diseases. Age, temperature (T), white blood cell (WBC), lymphocytes (LY), hematocrit (HCT), CRP, and finger pulse oxygen saturation (SpO2) may correlate with liver function impairment and may predict the occurrence and severity of liver function impairment. Some therapeutic drugs (like glucocorticoid) may be involved in the liver function impairment of COVID-19 patients. Most liver function indices improved significantly after active treatment. Although COVID-19 and other common respiratory infectious diseases share some clinical characteristics, COVID-19 has its own characteristics.

Efficacy and safety study of direct-acting oral anticoagulants for the treatment of chronic portal vein thrombosis in patients with liver cirrhosis.

AIMS: This study is designed to investigate the efficacy and safety of direct-acting oral anticoagulants (DOACs) for the treatment of chronic portal vein thrombosis (PVT) in liver cirrhosis patients. MATERIALS AND METHODS: In a prospective cohort study, patients were divided into DOACs group (oral rivaroxaban tablets or dabigatran etexilate capsules) and control group (no anticoagulant treatment). Based on propensity score matching method, 40 patients with cirrhosis and chronic PVT in each of the groups were recruited for this study. CT portal venography was used to monitor the portal vein area. Color Doppler ultrasound was used to monitor the portal vein flow rate. Biochemical testing and thromboelastography (TEG) were also used for monitoring the status of PVT. RESULTS: After 3 months of DOACs treatment, the complete/partial recanalization rate of DOACs was 12.8% (5/39). After 6 months of DOACs treatment, the PVT complete/partial recanalization rate of DOACs was 28.2% (11/39). The recanalization rate and portal vein flow velocity improvement were higher than those in the control group (P < 0.05). Patients' total bilirubin level and Child-Pugh scores were improved in the DOACs group. The TEG coagulation index was lower in the DOACs group than in the control group (P < 0.05). There was no statistically significant difference between the DOACs group and control group in the cases of bleeding (P > 0.05). CONCLUSION: DOACs are effective and safe for chronic PVT in patients with liver cirrhosis. The TEG can predict the risk of bleeding in patients with chronic PVT in cirrhosis, which is more sensitive than conventional coagulation function test.

Potential effects of Mina53 on tumor growth in human pancreatic cancer.

Myc-induced nuclear antigen (Mina53) is a protein with a molecular weight of 53 kDa expression of which is induced by c-Myc. Increased expression of Mina53 is documented in some human carcinomas. In this study, we found markedly increased Mina53 expression in pancreatic cancer tissue specimens. This expression did not correlate with clinicopathological characteristics, such as sex, age, and presence of distant metastasis. However, there was a statistically significant association with histological differentiation, TNM stage, and lymph node metastases. To study functional role of Mina53, we silenced its expression by siRNA in PANC-1 cells. These cells were arrested in the G2/M phase, and apoptosis rates were increased. In conclusion, increased expression of Mina53 may play an important role in the development of human pancreatic cancer. Mina53 can be used as a marker for pancreatic cancer and may potentially be exploited as a target for treatment of pancreatic cancer.

Proton pump inhibitor for non-erosive reflux disease: a meta-analysis.

AIM: To evaluate the efficacy, safety and influential factors of proton pump inhibitor (PPI) treatment for non-erosive reflux disease (NERD). METHODS: PubMed, MEDLINE, EMBASE and the Cochrane Library were searched up to April 2013 to identify eligible randomized controlled trials (RCTs) that probed into the efficacy, safety and influential factors of PPI treatment for NERD. The rates of symptomatic relief and adverse events were measured as the outcomes. After RCT selection, assessment and data collection, the pooled RRs and 95%CI were calculated. This meta-analysis was performed using the Stata 12.0 software (Stata Corporation, College Station, Texas, United States). The level of evidence was estimated by the Grading of Recommendations Assessment, Development and Evaluation system. RESULTS: Seventeen RCTs including 6072 patients met the inclusion criteria. The results of the meta-analysis showed that PPI treatment was significantly superior to H2 receptor antagonists (H2RA) treatment (RR = 1.629, 95%CI: 1.422-1.867, P = 0.000) and placebo (RR = 1.903, 95%CI: 1.573-2.302, P = 0.000) for the symptomatic relief of NERD. However, there were no obvious differences between PPI and H2RA (RR = 0.928, 95%CI: 0.776-1.110, P = 0.414) or PPI and the placebo (RR = 1.000, 95%CI: 0.896-1.116, P = 0.997) regarding the rate of adverse events. The overall rate of symptomatic relief of PPI against NERD was 51.4% (95%CI: 0.433-0.595, P = 0.000), and relief was influenced by hiatal hernia (P = 0.030). The adverse rate of PPI against NERD was 21.0% (95%CI: 0.152-0.208, P = 0.000), and was affected by hiatal hernia (P = 0.081) and drinking (P = 0.053). CONCLUSION: PPI overmatched H2RA on symptomatic relief rate but not on adverse rate for NERD. Its relief rate and adverse rate were influenced by hiatal hernia and drinking.

Hugl-1 induces apoptosis in esophageal carcinoma cells both in vitro and in vivo.

AIM: To determine whether the human giant larvae homolog 1 gene (Hugl-1/Llg1/Lgl1) exerts tumor suppressor effects in esophageal cancer. METHODS: We constructed a Hugl-1 expression plasmid, pEZ-M29-Hugl1, for gene transfection. We transfected the pEZ-M29-Hugl1 plasmid into Eca109 esophageal cancer cell lines with Lipofectamine 2000 to overexpress Hugl-1. Real-time reverse transcription-polymerase chain reaction (RT-PCR) and Western blotting were performed to determine the effects of the plasmid on Hugl-1 expression. In vitro cell proliferation and apoptosis were examined separately by cell counting Kit-8 (CCK-8) assay, flow cytometry, and Western blotting before and after the transfection of the plasmid into Eca109 cells. Cell cycle distribution was assessed with flow cytometry. The effect of Hugl-1 overexpressing on tumor growth in vivo was performed with a xenograft tumor model in nude mice. Expression of Hugl-1 in xenograft tumor was analyzed by immunohistochemistry. The transferase-mediated dUTP nick end-labeling (TUNEL) technique was performed to detect and quantitate apoptotic cell. RESULTS: The transfection efficiency was confirmed with real-time RT-PCR and Western blotting. Our results show that compared with control groups the mRNA levels and protein levels of Hugl-1 in pEZ-M29-Hugl1-treated group were remarkably increased (P < 0.05). The CCK-8 assay demonstrated that the growth of cells overexpressing Hugl-1 was significantly lower than control cells. Cell cycle distribution showed there was a G0/G1 cell cycle arrest in cells overexpressing Hugl-1 (64.09% ± 3.14% vs 50.32% ± 4.60%, 64.09% ± 3.14% vs 49.13% ± 2.24%). Annexin V-fluorescein isothiocyanate revealed that apoptosis was significantly increased in cells overexpressing Hugl-1 compared with control group (17.33% ± 4.76% vs 6.90% ± 1.61%, 17.33% ± 4.76% vs 6.27% ± 0.38%). Moreover, we found that Hugl-1 changes the level of the anti-apoptotic protein Bcl-2 and the pro-apoptotic protein Bax and the activation of both caspase-3 and caspase-9. With a TUNEL assay, we found that Hugl-1 markedly increased the apoptosis rate of Eca109 cells in vivo (60.50% ± 9.11% vs 25.00% ± 12.25%). It was shown that Hugl-1 represents a significantly more effective tumor suppressor gene alone in a xenograft tumor mouse model. This data suggest that Hugl-1 inhibited tumor growth and induced cell apoptosis in vivo. CONCLUSION: These results suggest that Hugl-1 induces growth suppression and apoptosis in a human esophageal squamous cell carcinoma cell line both in vitro and in vivo.