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Objective:To evaluate the value of preoperative prediction of vessel invasion (VI) of locally advanced gastric cancer by machine learning model based on the venous phase enhanced CT radiomics features.Methods:A retrospective analysis of 296 patients with locally advanced gastric cancer confirmed by pathology in the First Affiliated Hospital of Zhengzhou University from July 2011 to December 2020 was performed. The patients were divided into VI positive group ( n=213) and VI negative group ( n=83) based on pathological results. The data were divided into training set ( n=207) and test set ( n=89) according to the ratio of 7∶3 with stratification sampling. The clinical characteristics of patients were recorded, and the independent risk factors of gastric cancer VI were screened by multivariate logistic regression. Pyradiomics software was used to extract radiomic features from the venous phase enhanced CT images, and the minimum absolute shrinkage and selection algorithm (LASSO) was used to screen the features, obtain the optimal feature subset, and establish the radiomics signature. Four machine learning algorithms, including extreme gradient boosting (XGBoost), logistic, naive Bayes (GNB), and support vector machine (SVM) models, were used to build prediction models for the radiomics signature and the screened clinical independent risk factors. The efficacy of the model in predicting gastric cancer VI was evaluated by the receiver operating characteristic curve. Results:The degree of differentiation (OR=13.651, 95%CI 7.265-25.650, P=0.003), Lauren′s classification (OR=1.349, 95%CI 1.011-1.799, P=0.042) and CA199 (OR=1.796, 95%CI 1.406-2.186, P=0.044) were independent risk factors for predicting the VI of locally advanced gastric cancer. Based on the venous phase enhanced CT images, 864 quantitative features were extracted, and 18 best constructed radiomics signature were selected by LASSO. In the training set, the area under the curve (AUC) of XGBoost, logistic, GNB and SVM models for predicting gastric cancer VI were 0.914 (95%CI 0.875-0.953), 0.897 (95%CI 0.853-0.940), 0.880 (95%CI 0.832-0.928) and 0.814 (95%CI 0.755-0.873), respectively, and in the test set were 0.870 (95%CI 0.769-0.971), 0.877 (95%CI 0.788-0.964), 0.859 (95%CI 0.755-0.961) and 0.773 (95%CI 0.647-0.898). The logistic model had the largest AUC in the test set. Conclusions:The machine learning model based on the venous phase enhanced CT radiomics features has high efficacy in predicting the VI of locally advanced gastric cancer before the operation, and the logistic model demonstrates the best diagnostic efficacy.
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Objective@#To examine the effects of ursodeoxycholic acid combined with Traditional Chinese Medicine on biochemical response in patients with primary biliary cholangitis.@*Methods@#According to the method of receiving treatment, 197 patients with primary biliary cholangitis were divided into Traditional Chinese Medicine plus Western medicine group (93 cases, 47.2%) and Western medicine group (104 cases, 52.8%). From the baseline date, the combined group was treated with ursodeoxycholic acid plus traditional Chinese medicine decoction or Chinese patent medicine for at least one month and the Western medicine group simply took ursodeoxycholic acid . Additionally, Traditional Chinese medicine decoction prescriptions were mainly Xiaoyaosan and Yinchenhao. Chinese patent medicine were restricted to Biejia Ruangan tablets, Fuzheng Huayu capsules, Jiuweigantai capsules and Yinzhihuang capsules, which were used to treat liver fibrosis and cholestasis. The primary efficacy endpoint was defined as ALP level < 1.67 × ULN and ≥ 15% decrease in ALP with baseline level and TBIL≤ULN after 12 months of treatment.@*Results@#The overall biochemical response rate of patients was 35.0% (69/197). The response rate of TCM+ Western medicine group was 43.0% (40/93), and that of Western medicine group was 27.9% (29/104). The difference between the two groups was statistically significant (χ2 = 4.936, P < 0.05). Further analysis showed that the Chinese and Western medicine group was superior to the Western medicine group alone in reducing γ-glutamyltransferase (GGT) and TBiL [the median decline were GGT: 160.1 U/L and 111.3 U/L (Z = -2.474, P < 0.05), TBiL: 5.2 umol/l and 3.1 umol/l (Z = -2.125, P < 0.05)].@*Conclusion@#UDCA combined with TCM therapy can remarkably improve the biochemical response rate in patients with PBC and distinctly decrease the TBIL and GGT levels than UDCA monotherapy.
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BACKGROUND:Decreased function and reduced number of CD4+CD25+regulatory T cells have been considered the major manifestation of immunity dysfunction in children with primary nephrotic syndrome. Bone marrow mesenchymal stem cells have immunoregulation effects, which up-regulate CD4+CD25+regulatory T cells, inhibit proliferation of lymphocytes, and have been widely used in many immune diseases. OBJECTIVE:To investigate the effects of bone marrow mesenchymal stem celltransplantation on the CD4+CD25+regulatory T cells of peripheral blood in rats with primary nephrotic syndrome. METHODS:Bone marrow mesenchymal stem cells from six Sprague-Dawley rats were isolated, passaged and utilized for cellsuspension preparation. At the third passage, bone marrow mesenchymal stem cells were used for transplantation. The remaining 30 rats were randomly and equal y divided into three groups:normal group, normal saline infusion group, and bone marrow mesenchymal stem cells group. The rat models of primary nephrotic syndrome were established by single injection of adriamycin intravenously through tail vein in the latter two groups. Rats were then treated with bone marrow mesenchymal stem cells (1×10 7 ) (bone marrow mesenchymal stem cells group) or normal saline (normal saline infusion group) through tail vein at the same time after adriamycin administration. The normal group received no treatment. RESULTS AND CONCLUSION:Compared with the normal group, rats in the normal saline infusion group developed nephropathy characterized by ascites, proteinuria, hypoalbuminemia, hypercholastero-lnemia, and progressive renal injury. However, the proteinurine and clinical severity in bone marrow mesenchymal stem cells group were significantly ameliorated after treatment with bone marrow mesenchymal stem cells. CD4+CD25+Treg/CD4+Treg in the peripheral blood in the bone marrow mesenchymal stem cells group and normal saline infusion group were significantly higher than that in the normal group at 28 days after model establishment (P0.05). The expression of FoxP3 mRNA in the peripheral blood mononuclear cells of the bone marrow mesenchymal stem cells group was significantly higher than that in the normal saline infusion group and normal group (P<0.05). The bone marrow mesenchymal stem cells play a protective effect in rats with primary nephrotic syndrome, which may be related to the increase of local expression of FoxP3 and generation of CD4+CD25+Treg.
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Objective Percutaneous coronary intervention( PCI) is effective in improving the ischemia and prognosis of pa-tients with acute myocardial infarction ( AMI) to reduce the short-term mortality.However, little research has been done on PCI in eld-erly AMI patients.The study aimed to evaluate the efficacy and the safety of percutaneous coronary intervention in elderly AMI patients (≥75 years old) . Methods 213 AMI patients who underwent emergency PCI in Jingling Hospital from January 2012 to December 2013 were divided into 2 groups:elderly group (≥75 years old, n=57) and non-elderly group (<75years old,n=156).Retrospec-tive analysis were made on the clinical data and the coronary intervention features of the patients. Results There were more patients having dyspnea, fatigue and other heart failure symptoms at the onset of first-break AMI in elderly group than in non-elderly group (21.1%vs 3.2%,P<0.0).More women (47.4% vs 16.7%,P<0.01) and more patients with hypertention or diabetes mellitus were found in elderly group.The procedure success rates with TIMI-3 flow grade of post-PCI in both groups were very high (100%). Compared with non-elderly group, the occurrence of the procedure-related complications (3.5%vs 2.6%,P=NS) and major adverse cardiac event rates (8.8%vs 6.4%,P=NS) and in-hospital mortality (5.3%vs 2.6%,P=NS) showed no significant difference.Conclusion There are more atypical clinical symptoms in elderly AMI patients. The emergency PCI in elderly AMI patients can effectively make artery unimpeded with high successful rate, few com-plications and a favorable short-term prognosis.
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ObjectiveTo investigate the role of MG-132, a specific dipeptide proteasome inhibitor, on the proliferation, apoptosis and the related proteins in renal interstitial fibroblasts. MethodsRenal interstitial fibroblasts (NRK-49F) were induced by transforming growth factor β1 (TGF-β1, 5 μg/L) and pro-treated with MG-132 (0～5 μmol/L). The cell proliferation was measured with MTT method. Cell cycle and apoptosis were analyzed by flow cytometry. The apoptosis was also analyzed by Annexin V/PI staining and DNA ladder. Expression of p53, p27, p21, caspase-3, Bcl-2 and Bax protein was examined by Western blot. ResultsTGF-β1 (5 μg/L) could stimulate the proliferation of NRK-49F. MG-132 (0.25～5 μmol/L) could inhibit TGF-β1-induced proliferation in a dose-dependent manner through G1-arrest. TGF-β1 alone could not induce apoptosis (3.880%±0.365% vs 4.723%±1.582%). But pretreatment of MG-132 (0.1～2.5 μmol/L) could significantly induce apoptosis of TGF-β1-stimulated NRK-49F in a dose-dependent manner. Typical DNA ladder was also confirmed in these two groups in the DNA fragments analysis after being incubated with 2.5 μmol/L MG-132 with or without 5 μg/L TGF-β1. Western blot showed that MG-132 could activate the cell-cycle and apoptosis-related proteins such as p53, p21, caspase-3, Bax and inhibit Bcl-2 in a dose-dependent manner, while expression of p27 remained unchanged. ConclusionsProteasome inhibitor MG-132 can inhibit proliferation and induce the cell apoptosis in renal interstitial fibroblasts stimulated by TGF-β1. The mechanism may be associated to the mediation of p53, p21, caspase-3, Bcl-2 and bax pathways. Protoasome inhibitor may be a new strategy to treat renal interstitial fibrosis.
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Objective To investigate the changes of expression of peroxisome proliferator-activated receptor γ (PPARγ) and its coregulators and monocyte chemotactic factor (MCP-1) treated with intedeukin-1β (IL-1β), and to analyze the mechanism of interaction of these factors. Methods Renal tubular cells (HK-2 cells) were cultured in vitro. Total cellular RNA was isolated for real-lime quantitative polymerase chain reaction (real-time PCR), nuclear extracts were prepared for Western blot analysis and EMSA. The supernatant was collected for ELISA after the treatment of IL-1β at different concentrations and time points. Results Under stimulus of different concentrations of IL-1β (0～20 μg/L) for 24 hours, the mRNA expression of PPARγ, SRC-1, SRC-2 and PGC-1 decreased significantly (P<0.05), meanwhile NCoR increased obviously (P<0.05). In further time-dependent experiment, the mRNA levels of SRC-2 and PGC-1 decreased by 57% and 48%, respectively, at 1 hour after treatment with 10 μg/L IL-1β (P<0.05). The expression of SRC-1 decreased by 43%only after 2 hours (P<0.05). The expression of NCoR was not obviously changed until stimulated by IL-1β for 8 hours (2.17 folds, P<0.05), then it decreased slowly. In the same time-dependent experiment, Western blot analysis showed that IL-1β (10 μg/L) significantly decreased the protein level of PPARγ at 4 hours (P<0.05). ELISA analysis revealed that the secretion of MCP-1 kept on rising and reached the peak (160.56±2.80) ng/L at 8 hours (P<0.01), then decreased to (50.82±1.25) ng/L at 24 hours (P<0.01). IL-1β could down-regulate the DNA binding activity of PPARγ, and the activity of NF-κB was up-regulated. Conclusions PPARγ and its eoregulators are closely related to MCP-1 and NF-κB during inflammation response in kidney. The activation of NF-κB by IL-1β leads to the decrease of PPARγ, and its coactivators expression levels, however the expression of MCP-1 and NCoR in renal tubular epithelial cells is up-regulated. PPARγ together with its coregulators participate in the inflammation response in kidney.