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.
It has been found that in biological studies, the simple linear superposition mathematical model cannot be used to express the feature mapping relationship from multiple activated grid cells' grid fields to a single place cell's place field output in the hippocampus of the cerebral cortex of rodents. To solve this problem, people introduced the Gauss distribution activation function into the area. We in this paper use the localization properties of the function to deal with the linear superposition output of grid cells' input and the connection weights between grid cells and place cells, which filters out the low activation rate place fields. We then obtained a single place cell field which is consistent with biological studies. Compared to the existing competitive learning algorithm place cell model, independent component analysis method place cell model, Bayesian positon reconstruction method place cell model, our experimental results showed that the model on the neurophysiological basis can not only express the feature mapping relationship between multiple activated grid cells grid fields and a single place cell's place field output in the hippocampus of the cerebral cortex of rodents, but also make the algorithm simpler, the required grid cells input less and the accuracy rate of the output of a single place field higher.
Objective To introduce the basic information about mad cow disease and the current status of safety control of medical devices derived from mammalian animal tissues. Methods Literature concernedwas reviewed intensively. Results Mad cow disease, also knownas bovine spongiform encephacitis (BSE)， is generally considered from the samesource of Scrapie, and they are caused by the same kind of sponginess brain tissue pathological changes. Mad cow disease is caused by the misfolding of a small protein called Prion. This disease has the character of slowly breaking down the central neuron system of animals. Conclusion Further researches can provide evaluation for safety considerations of medical devices deriving from animal.
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.
Rheumatoid arthritis (RA) is a chronic autoimmune disease remarkably characterized by synovitis of joints, whose pathogenesis is complicated and not yet fully elucidated. A variety of cells, cytokines and intercellular signaling pathways are involved in the occurrence and development of RA. The mitogen activation protein kinase (MAPK) signaling pathway is closely related to the pathogenesis of RA, and plays an important role in the formation of pannus, synovitis, and bone destruction. This paper reviews the research progress of MAPK signaling pathway in RA from the aspects of the interaction of MAPK signaling pathway with a variety of key cells and cytokines in the pathogenesis of RA, in order to provide a direction and theoretical basis for anti-RA drug therapy research.
Calnexin is a lectin-like molecular chaperone protein on the endoplasmic reticulum, mediating unfolded protein responses, the endoplasmic reticulum Ca2+ homeostasis, and Ca2+ signals conduction. In recent years, studies have found that calnexin plays a key role in the heart diseases. This study aims to explore the role of calnexin in the activation of cardiac fibroblasts. A transverse aortic constriction (TAC) mouse model was established to observe the activation of cardiac fibroblasts in vivo, and the in vitro cardiac fibroblasts activation model was established by transforming growth factor β1 (TGFβ1) stimulation. The adenovirus was respectively used to gene overexpression and silencing calnexin in cardiac fibroblasts to elucidate the relationship between calnexin and cardiac fibroblasts activation, as well as the possible underlying mechanism. We confirmed the establishment of TAC model by echocardiography, hematoxylin-eosin, Masson, and Sirius red staining, and detecting the expression of cardiac fibrosis markers in cardiac tissues. After TGFβ1 stimulation, markers of the activation of cardiac fibroblast, and proliferation and migration of cardiac fibroblast were detected by quantitative PCR, Western blot, EdU assay, and wound healing assay respectively. The results showed that the calnexin expression was reduced in both the TAC mice model and the activated cardiac fibroblasts. The overexpression of calnexin relieved cardiac fibroblasts activation, in contrast, the silencing of calnexin promoted cardiac fibroblasts activation. Furthermore, we found that the endoplasmic reticulum stress was activated during cardiac fibroblasts activation, and endoplasmic reticulum stress was relieved after overexpression of calnexin. Conversely, after the silencing of calnexin, endoplasmic reticulum stress was further aggravated, accompanying with the activation of cardiac fibroblasts. Our data suggest that the overexpression of calnexin may prevent cardiac fibroblasts against activation by alleviating endoplasmic reticulum stress.
Objective To investigate the expression of fibroblast activation protein( FAP) in mouse pulmonary fibrosis and the relationship between FAP and trarisforming growth factor β1 ( TGF-β1 ) .Methods The mouse model with pulmonary fibrosis was established by intratracheally instillation of bleomycin. The expressions of FAP, α-smooth muscle action( α-SMA) , and TGF-β1 in lung tissues were detected with immunohistochemical technique. Results There was no expression of FAP in the normal lung tissue. In the pulmonary fibrosis mice, FAP was found in the fibroblasts existed in bronchiolar adventitia or peribronchiolar ( and perivascular) connective tissue. In the fibroblast foci, the localizations of α-SMA, TGF-β1 , and FAP were similar, but the expression of FAP was more extensive than that of α-SMA and ber than that ofTGF-β1 . The degree of lung fibrosis was bly correlated with FAP, α-SMA, and TGF-β1 ( r = 0. 795,0. 766,0. 628; P lt; 0. 01) . A significantly positive correlation was also observed between TGF-β1 and FAP( r =0. 706, P lt; 0. 01) . Conclusions FAP is especially expressed in the fibroblast foci in pulmonaryfibrosis and bly correlated with the severity of pulmonary fibrosis. FAP and TGF-β1 possibly play a synergistic role in the progression of pulmonary fibrosis.
The cleft lip and palate (CLP) is one of the most common craniofacial malformations in humans. We collected functional magnetic resonance data of 23 CLP patients before rehabilitation training (Bclp) and 23 CLP patients after rehabilitation training (Aclp), who were performing Chinese character pronunciation tasks, and performed brain activation analysis to explore the changes of brain mechanism in CLP patients after articulation disorder rehabilitation training. The study found that Aclp group had significant activation in the motor cortex, Broca area, Wernicke area and cerebellum. While the Bclp group had weak activation in the motor cortex with a small activation range. By comparing the differences and co-activated brain regions between the two groups, we found that rehabilitation training increased the activity level of negatively activated brain areas (cerebellum, left motor area, Wernicke area, etc.) to a positive level. At the same time, the activity level of weakly activated brain areas (right motor area, Broca area, etc.) was also increased. Rehabilitation training promoted the activity level of articulation-related brain regions. So that the activation intensity of articulation-related brain regions can be used as a quantifiable objective evaluation index to evaluate the effect of rehabilitation training, which is of great significance for the formulation of rehabilitation training programs.
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.
Platelets are rapidly activated by activators and produce a large number of platelet microparticles (PMPs) with high coagulation activity, resulting in coagulation dysfunction. However, the generation mechanism of PMPs is still not clear. Hopping probe ion conductance microscopy (HPICM) has special technical advantages in non-contact, real-time, high-resolution imaging of living cells under physiological conditions. Using HPICM, this study monitored the processes of platelet activation and generation of PMPs in real time in the presence of calcium ionophore A23187 and cytochalasin D (CD), respectively. The results proved that the intracellular calcium concentration and the cytoskeletal proteins played important roles in the platelet activation and the generation of PMPs. Compared with the low density spread shape platelets (LDSS), the high density bubble shape platelets (HDBS) were more sensitive to the calcium ionophore A23187 and cytochalasin D. This research has a guiding significance for the further study on the relationship between platelet activation and coagulation function using HPICM.