ObjectiveTo observe the effect of complement receptor 1 (CR1) on barrier of cultured human retinal epithelial cells (hRPE) under complement-activated oxidative stress.
MethodsThe third to fifth passage of hRPE cultured on Transwell insert were used to establish a stable hRPE monolayer barrier. The hRPE monolayer barrier was exposed to 500 μmol/L ten-butyl hydroperoxide and 10% normal human serum to establish the hRPE monolayer barrier model of complement-activated oxidative stress in vitro. hRPE monolayer barriers under complement-activated oxidative stress were divided into two groups including model group and CR1 treatment (1 μg/ml) group. Model group and CR1 treatment group were treated with 1 μl phosphate buffer solution (PBS) or CR1 for 4 hours. Normal hRPE monolayer barrier were used as control in transepithelial resistance (TER) measurement experiment. TER was measured to evaluate the barrier function of hRPE. The hRPE-secreted vascular endothelial growth factor (VEGF) and chemokine (C-C Motif) Ligand 2 (CCL2), together with complement bioactive fragments (C3a, C5a) and membrane-attack complex (MAC) in the supernatant were detected by enzyme-linked immune sorbent assay.
ResultsStable hRPE monolayer barrier was established 3 weeks after hRPE seeded on Transwell insert. Complement-activated oxidative stress resulted in a sharp decrease of TER to 54.51% compared with normal hRPE barrier. CR1 treatment could significantly improve TER of barrier under complement-activated oxidative stress to 63.48% compared with normal hRPE barrier(t=21.60, P < 0.05). Compared with model group, CR1 treatment could significantly decrease the concentration of VEGF and CCL2 by 11.48% and 23.47% secreted by hRPE under complement-activated oxidative stress (t=3.26, 2.43; P < 0.05). Compared with model group, CR1 treatment could also decreased the concentration of C3a, C5a and MAC by 24.00%, 27.87%, 22.44%.The difference were statistically significant (t=9.86, 2.63, 6.94; P < 0.05).
ConclusionsCR1 could protect the barrier function of hRPE cells against complement-activated oxidative stress. The underlying mechanism may involve inhibiting complement activation and down-regulating the expression of VEGF and CCL2.
Objective
To clarify incidence and risk factors of hepatitis B reactivation during short term (one month) in hepatitis B virus (HBV) related hepatocellular carcinoma (HCC) patients receiving partial hepatectomy.
Methods
From January 2015 to December 2015, 214 consecutive patients with HBV-related HCC who underwent partial hepatectomy were retrospectively enrolled in this study. The risk factors affecting incidence of hepatitis B reactivation were analyzed.
Results
Hepatitis B reactivation happened in 7.0% (15/214) of patients within 1 month after partial hepatectomy. By univariate analysis, the preoperative HBV-DNA negativity and hepatitis B e antigen (HBeAg) positivity were significantly correlated with the occurrence of hepatitis B reactivation (P=0.023 and P=0.001, respectively). By multivariate analysis, the preoperative HBV-DNA negativity 〔OR=9.21, 95% CI (2.40, 35.45), P=0.001〕 and HBeAg positivity 〔OR=20.51, 95% CI (5.41, 77.73), P<0.001〕 were the independent risk factors for hepatitis B reactivation.
Conclusions
Hepatitis B reactivation is common after partial hepatectomy for HBV-related HCC during short term, especially in patients whose preoperative HBV-DNA negativity and HBeAg positivity. A close monitoring of HBV-DNA during short term after partial hepatectomy is necessary, once hepatitis B is reactivated, antiviral therapy should be given.
Drugs may induce hepatitis B virus (HBV) reactivation (HBV-R). Here we have reviewed the definition and harm of HBV-R, the risk drugs and their underlying mechanism, the influence factors, as well as the early intervention measures. It is shown that multiple drugs, including chemotherapy drugs, immunotherapy drugs, directly acting antivirals, cell therapy, etc., can induce HBV-R by affecting host immunity or directly activating HBV transcription factors. HBV-R could cause severe liver damage, even interruption of treatment of original diseases, affecting the prognosis of patients. Through precisely identifying risk drugs, monitoring the influence factors, and prescribing preventive anti-HBV regimen if necessary, the incidence of HBV-R can be significantly reduced. It is also suggested that clinical physicians should not only pay attention to the early identification and intervention of HBV-R, but also further study the mechanism of HBV-R in depth, especially the underlying mechanism between host, HBV and risk factors. This will help to promote the discovery of more valuable markers for risk prediction and targets for early intervention, and to further reduce the risk of HBV-R and improve the prognosis of patients.
Objective To further strengthen the understanding of the genesis of thyroid tumors through the analysis of thyroid nodules in the clonal origin. Method The related literatures which discussed the clonality of thyroid nodules were reviewed and analyzed. Results About the clonal origin of thyroid nodules， the X chromosome inactivation detection and single gene mutation detection were the most widely chosen one at present. Most of the materials available at present related to X chromosome inactivation proposed that major part of the thyroid nodules were monoclonal and the malignant cells spreaded by means of the inner lymphatic vessel net，whereas polyclonal and monoclonal thyroid nodules coexisted occasionally. Only BRAF mutation was found of certain importance in clonal origin identification in the thyroid nodules. Conclusions Thyroid nodule is prevalent in clinical practice，while the clonality of thyroid nodules especially the thyroid tumor is not clear. And for the time being the commonly used methods to identify the clonal origin of thyroid nodule are X chromosome inactivation and single gene mutation detection. Published results confirm the finding of X chromosome inactivation methods that the majority of thyroid nodules are monoclonally originated.
【Abstract】 Objective To discuss the role of leukocyte activation and inflammatory processes in the disease of chronic venous insufficiency （CVI）. Methods The relevant literatures about the role of leukocyte activation and inflammatory reaction in CVI were reviewed. Results The role of inflammatory reaction in occurrence and development of venous diseases has been studied a lot in recent years. It was found that the leukocyte activation and inflammatory reaction are involved in the structural remodeling of venous valves and walls, leading to valvular incompetence and formation of varicose veins. Conclusion Leukocyte activation and inflammatory processes take important roles in the occurrence and progression of CVI.
Event-related desynchronization (ERD) is the basic feature of electroencephalogram (EEG), and the brain-computer interface based on motor imagery (MI-BCI) with the foundation of the analysis of ERD is of great significance in motor function recovery. The valid ERD characteristics extracted from EEG are the key to the performance of the BCI, so the study of which kind of stimulation mode can prompt subjects to generate more obvious characteristics of ERD is crucial. Four different stimulation modes are designed in this paper, and the effects of motion imagery tasks under static text stimulation, grip video stimulation, serial motion video stimulation of fingers as well as serial motion video stimulation of fingers with sound on the characteristics of ERD are analyzed. Combining the analysis of time-frequency spectrum, the power spectral density curve, ERD value and brain topographic map, it is shown that the ERD under serial motion video stimulation of fingers and serial motion video stimulation of fingers with sound modes is much stronger and has wider range of activation, and the BCI based on the analysis of ERD will have a better effect on practical application. As a result, the recognition and acceptance of the users of BCI system are improved in some extent.
Objective To verify the technics of inactivating/removing pathogens in medical chitosan derived from shrimp shell. Methods Possible pathogen species were included according to the raw material of shrimp shell used in production, then bacillus cereus, porcine parvovirus (PPV) and pseudorabies virus (PRV) were selected as indicator pathogens.Pathogen solution was prepared in accordance with Technical Standard for Disinfection. The processing procedure of medical chitosan was analyzed to determine whether the alkal ization of chitin and the filter steril ization of chitosan were capable of inactivating/removing pathogens and their efficiencies were tested. Results Bacillus cereus was removed by 8 184 cfu/ mL after alkal ization and 30 818 cfu/mL after filter steril ization. The average logarithm inactivation value (LIV) of PPV and PRV after alkal ization were equal to or above 4.76 logTCID50/0.1 mL and 6.67 logTCID50/0.1 mL, respectively, and their average LIV after filter steril ization were 2.25 logTCID50/0.1 mL and 3.04 logTCID50/0.1 mL. The alkal ization of chitin inactivated/removed indicator pathogens effectively, while the filter steril ization of chitosan removed bacterial effectually but could not inactivate viruses completely. Conclusion The alkal ization of chitin can be used as the technics of inactivating/removing pathogens during the preparation process of medical chitosan to guarantee the safety of the product.
ObjectiveTo systematically review the efficacy of different nucleosides (acids) in preventing hepatitis B virus reactivation after chemotherapy in cancer patients. MethodsThe Cochrane Library, PubMed, EMbase, Web of Science, CNKI, WanFang Data, and VIP databases were electronically searched to collect randomized controlled trials (RCTs) of different nucleosides (acids) to prevent HBV reactivation after chemotherapy in cancer patients from inception to June 7th, 2021. Two reviewers independently screened literature, extracted data, and assessed the risk of bias of included studies. Network meta-analysis was then performed by using Stata 16.0 software. ResultsA total of 43 RCTs involving 3 269 patients were included. There were 7 interventions, namely entecavir (ETV), lamivudine (LAM), adefovir dipivoxil (ADV), telbivudine (LdT), tenofovir dipivoxil (TDF), lamivudine combined with entecavir (LAM+ETV), and lamivudine combined with adefovir dipivoxil (LAM+ADV). The results of network meta-analysis showed that the efficacy of reducing the reactivation rate of ETV, LAM, ADV, LdT, TDF, LAM+ETV, LAM+ADV were superior than the control group. The ETV, LAM and ADV were not as effective as LAM+ETV. The leading drug combinations were LAM+ETV (94.8%), LdT (81.5%) and LA+ADV (58.0%). ConclusionsCurrent evidence shows that LAM+ETV, LdT, and LA+ADV are more effective in preventing hepatitis B virus reactivation after chemotherapy in cancer patients. Due to limited quality and quantity of the included studies, more high-quality studies are required to verify the above conclusions.
Long non-coding RNA (lncRNA) Dnm3os plays a critical role in peritendinous fibrosis and pulmonary fibrosis, but its role in the process of cardiac fibrosis is still unclear. Therefore, we carried out study by using the myocardial fibrotic tissues obtained by thoracic aortic constriction (TAC) in an early study of our group, and the in vitro cardiac fibroblast activation model induced by transforming growth factor-β1 (TGF-β1). Quantitative real-time polymerase chain reaction (RT-qPCR), Western blot, and collagen gel contraction test were used to identify the changes of activation phenotype and the expression of Dnm3os in cardiac fibroblasts. Small interfering RNA was used to silence Dnm3os to explore its role in the activation of cardiac fibroblasts. The results showed that the expression of Dnm3os was increased significantly in myocardial fibrotic tissues and in the activated cardiac fibroblasts. And the activation of cardiac fibroblasts could be alleviated by Dnm3os silencing. Furthermore, the TGF-β1/Smad2/3 pathway was activated during the process of cardiac fibroblasts activation, while was inhibited after silencing Dnm3os. The results suggest that Dnm3os silencing may affect the process of cardiac fibroblast activation by inhibiting TGF-β1/Smad2/3 signal pathway. Therefore, interfering with the expression of lncRNA Dnm3os may be a potential target for the treatment of cardiac fibrosis.
ObjectiveTo explore whether platelet activation is associated with systemic inflammatory responses.
MethodsWe conducted a cross-sectional study to enroll all aortic dissection (AD) patients (AD group) from January 1, 2015 to June 30, 2015 in the Emergency Department. According to the characteristics of AD patients, we matched hypertension (hypertension group) and health participants (health group) with AD patients at a proportion of 1:1:1. Blood samples were collected on admission for blood routine test [mean platelet volume (MPV)/platelet (PLT)] and inflammatory cytokines [tumor necrosis factor (TNF)-α and interleukin (IL)-6] analysis. We compared all parameters among the three groups and performed bivariate correlation analyses.
ResultsExpressions of TNF-α and IL-6 in the AD group [(20.9±4.5), (168.8±75.1) pg/mL] were significantly higher than those in the hypertension group [(4.3±1.9), (8.4±2.9) pg/mL] and healthy group [(5.4±1.6), (8.7±3.8) pg/mL] (P＜0.05). MPV/PLT in the AD group was significantly higher than that in the hypertension group and healthy group (0.106±0.035 vs 0.049±0.010, P＜0.05; 0.106±0.035 vs 0.054±0.019, P＜0.05). There were positive correlations between MPV/PLT and TNF-α (r=0.516, P=0.002), and between MPV/PLT and IL-6 (r=0.633, P＜0.001) in the AD group.
ConclusionIn summary, our study shows that platelets of AD patients can be activated, and the degree of activation is associated with systemic inflammatory responses.
