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OBJECTIVES@#To study the value of autotaxin (an autocrine motility factor) level in serum and bronchoalveolar lavage fluid (BALF) in predicting refractory Mycoplasma pneumoniae pneumonia (RMPP) in children and its correlation with interleukin-6 (IL-6), interleukin-8 (IL-8), and C-reactive protein (CRP).@*METHODS@#A retrospective analysis was performed on 238 children with Mycoplasma pneumoniae pneumonia who were admitted from January 2019 to December 2021. According to disease severity, they were divided into two groups: RMPP (n=82) and general Mycoplasma pneumoniae pneumonia (GMPP; n=156). The two groups were compared in terms of the levels of autotaxin, IL-6, IL-8, and CRP in serum and BALF to study the value of autotaxin level in serum and BALF in predicting RMPP in children, as well as the correlation of autotaxin level with IL-6, IL-8, and CRP in children with RMPP.@*RESULTS@#Compared with the GMPP group, the RMPP group had significantly higher levels of autotaxin, IL-6, IL-8, and CRP in serum and BALF (P<0.05). For the children with RMPP, the levels of autotaxin, IL-6, IL-8, and CRP in serum and BALF in the acute stage were significantly higher than those in the convalescent stage (P<0.05). The receiver operating characteristic (ROC) curve showed that the level of autotaxin in serum and BALF had a good value in predicting RMPP in children, with an area under the curve of 0.874 (95%CI: 0.816-0.935) and 0.862 (95%CI: 0.802-0.924), respectively. The correlation analysis showed that the level of autotaxin in serum and BALF was positively correlated with IL-6, IL-8, and CRP levels (P<0.001).@*CONCLUSIONS@#The level of autotaxin in serum and BALF increases and is correlated with the degree of disease recovery and inflammatory cytokines in children with RMPP. Autotaxin can be used as a predictive indicator for RMPP in children.
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Criança , Humanos , Proteína C-Reativa , Citocinas , Interleucina-6 , Interleucina-8 , Mycoplasma pneumoniae , Pneumonia por Mycoplasma/diagnóstico , Estudos RetrospectivosRESUMO
Though incidence of Colorectal carcinoma is relatively less in consideration of world wide data, Indian scenario differs in higher incidence of Grade 3 carcinoma with signet ring cell component. We tried to find association between intercellular adhesion and propagation of cancer cell in Adenocarcinoma of Colorectal region. E-cadherin (ECAD) is the strongest intercellular adhesion molecule of epithelial cells and Autocrine Motility Factor (AMFR) is known propagator of cancer cell. We studied simultaneous immunohistochemical expression of these two molecules in 92 already diagnosed cases that were treated surgically by Colectomy or Abdomino Pelvic Resection. Normal Colorectal mucosa reacted strongly with ECAD and weakly with AMFR. With increasing dedifferentiation of the tumor, reversal manifested- more aggressive grades showed varied expression in comparison to its less aggressive type. Gastric 3 adenocarcinoma show weak ECAD (83% vs. 35%) and more AMFR (93% vs. 35%) expression in comparison to Grade 1. Weak ECAD and strong AMFR was also associated with increase in depth of tumor invasion. As ECAD and AMFR is at least partially responsible for varying histologic grade and behavioral pattern of colorectal adenocarcinoma, simultaneous evaluation of both parameters is helpful to understand pathway of progression of such cancer cell.
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Though incidence of Colorectal carcinoma is relatively less in consideration of world wide data, Indian scenario differs in higher incidence of Grade 3 carcinoma with signet ring cell component. We tried to find association between intercellular adhesion and propagation of cancer cell in Adenocarcinoma of Colorectal region. E-cadherin (ECAD) is the strongest intercellular adhesion molecule of epithelial cells and Autocrine Motility Factor (AMFR) is known propagator of cancer cell. We studied simultaneous immunohistochemical expression of these two molecules in 92 already diagnosed cases that were treated surgically by Colectomy or Abdomino Pelvic Resection. Normal Colorectal mucosa reacted strongly with ECAD and weakly with AMFR. With increasing dedifferentiation of the tumor, reversal manifested- more aggressive grades showed varied expression in comparison to its less aggressive type. Gastric3 adenocarcinoma show weak ECAD (83% vs. 35%) and more AMFR (93.% vs. 35%) expression in comparison to Grade1.Weak ECAD and strong AMFR was also associated with increase in depth of tumor invasion. As ECAD and AMFR is at least partially responsible for varying histologic grade and behavioral pattern of colorectal adenocarcinoma, simultaneous evaluation of both parameters is helpful to understand pathway of progression of such cancer cell.
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Objective: To investigate the down-regulation of phosphoglucose isomerase/autocrine motility factor (PGI/AMF) gene expression by interfering RNA for study on the pharmacological effect of PGI/AMF with ginsenoside Rh2 on leukemia KG1α cells. Methods: The KG1α and the silencing PGI/AMFα KG1α (siPGI-KG1α) cells at logarithmic growth phase were divided into control and drug groups in different dosages. The cells in the control group were normally treated and the cells in the drug groups were incubated with ginsenoside Rh2 in the concentration of 30, 45, 60, 75, and 90 μmol/L in 24, 48, and 72 h respectively. Cell Counting Kit-8 (CCK-8) was used to demonstrate the effect of ginsenside Rh2 on proliferation of KG1α and siPGI-KG1α cells. Trypan blue staining was applied to detecting the effect of human PGI on the proliferation of leukemia KG1α cell. The changes of KG1α by ginsenoside Rh2 on Akt pathway were tested by Antibody Array. The corelation of down-regulating PGI/AMF and Rh2 about mTOR, Raptor, and Rag was detected by Western blotting. Results: Compared with the control group, ginsenoside Rh2 had significant inhibition on the proliferation of KG1α. Down-regulation of PGI/AMF could make KG1α more sensitive to ginsenoside Rh2 and down-regulation of PGI could inhibit the proliferation of KG1α. Antibody Array showed that ginsenoside Rh2 could inhibit the proliferation of KG1α cells through decreasing the expression of P38, mTOR, Akt, AMPKα, PARP, and Bad. Western blotting results indicated that down-regulation of PGI through the synergy of mTOR, Rag, and Raptor with ginsenoside Rh2 could inhibit the proliferation of KG1α cells. Conclusion: Down-regulation of PGI/AMF coordinated with ginsenoside Rh2 could inhibit the proliferation of KG1α cells.
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ObjectiveTo investigate the expression of autocrine motility factor receptor (AMFR)in papillary thyroid carcinoma and its relationship with clinical characteristics of this disease.Methods Real - time quantitative PCR and immunohistochemical methods were used to analyze the expression of AMFR in papillary thyroid carcinomas.ResultsThe significant differences in AMFR expression between papillary thyroid carcinoma and normal thyroid tissues were found in the levels of mRNA (6.296 ± 1.568 vs 7.913 ± 2.351,t=3.681,P=0.001 ) and protein ( 63.1% vs 34.5 %,x2=13.722,P < 0.001 ),respectively.Immunohistochemistry analyses showed that the protein expression of AMFR in papillary thyroid carcinomas were significantly correlated with tumour size ( x2=5.209,P < 0.05 ) and lymph node metastasis ( x2=4.32,P < 0.05 ),and it was affected by the factors age ( x2=0.739,P=0.39 ) and gender ( x2=0.064,P=0.81 ).ConclusionsThe increased AMFR in papillary thyroid carcinoma would be a new target for cancer therapy and a new marker for prognosis.
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Autocrine motility factor (AMF) plays an important role in the stimulation of the migration and motility of cells, especially the generation, migration and angiogenesis of tumor. Recently, it has been found that AMF has three isoforms, ATX-t, ATX-m and PD-I alpha. The PD-I alpha isoform is specifically expressed in the brain, which plays extensive functions in nervous system, such as regulating neural development and differentiation, promoting neurotrauma repair, inducing neuropathic pain, even contributing neurodegeneration under some circumstances. This indicates the close relationship of AMF/AMFR and the pathophysiology of the nervous system. This paper mainly reviews the function of AMF and AMFR and its possible mechanism in the nervous system.
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Objective To explore a safe and high efficiency way of gene transfection of autocrine motility factor(AMF) in order to provide experimental basis for transplantation of myoblasts carrying AMF gone. Methods Sprague Dawley rat myoblasts were cultured, purified, proliferated and immunohisto-chemically verified. Then, the myoblasts were transfected with AMF and eGFP (enhanced green fluores-cent protein) gene by FIV (feline immunodeficiency virus). Fluorescence microscope and laser scanning confocal microscope were employed to detect eGFP so as to verify positive transfection rate. Expression of AMF was detected by immunohistochemical method. Results Myoblasts with 98% purity could he ob-tained after two weeks of primary culture and purification. Positive transfection rate reached 90.4% when MOI (multiplicity of infection) was 100 (P <0.01). The transfected AMF gene could express normally. Conclusions Explant culture is a proper way in rat myoblast culture. Meanwhile, AMF gene can he effectively transfected into rat myoblast and well expressed via FIV.
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Objective To study the clinical significance of tumor markers combined assay in the differential diagnosis of pleural effusion.Methods 165 serum and hydrothorax samples were collected from 165 in-patients with pleural effusion.Among them ,55 patients were suffered from malignant pleural effusion and 110 patients with benign pleural effusion.The concentration of CEA,and TSGF were determined by chemiluminescence assay.Results In malignant pleural effusion group,the positive rates of serum CEA and TSGF were 58.8% and 54.3% respectively,the positive rates of hydrothorax CEA and TSGF were 75.8% ,70.7% respectively.Among them,CEA and TSGF in malignant group were significantly higher than that in benign pleural effusion group(P < 0.01 ).So as did of the concentration.The sensitivity of combined assay with serum TSGF in diagnosing malignant pleural effusion was 85.7% ,with the specificity of 97.8%.Conclusion Tumor markers of CEA and TSGF have high clinical values in the differential diagnosis of pleural effusion.The combined assay with TSGF is recommended.