Objective To investigate the clinical value in differential diagnosis of benign and malignant breast mass.Methods One hundred and eighty three breast mass patients confirmed by pahthology,including 68 benign cases and 115 malignant cases,were retrospectively analyzed.The sonogram and blood flow of the mass were compratively analyzed.The blood flow parameter RI which detected by pulse wave Doppler were also compratively analyzed.Results Shapes,margins,posterior attenuation,L/T ratio,and microcalcification showed the significant differences between benign and malignant mass patients(P0.05).RI0.7 were in the malignant mass.Lymphadenectasis were found in 38 malignant caeses,and lymph node reactive hyperplasia were found in the 9 benign patients.Conclusion Color Doppler ultrasound can differentiate benign and malignant breast mass,it has important value in clinical application.
Object. Osteosarcoma is an intractable malignant disease, and few therapeutic methods can thoroughly eradicate its focuses. This study attempted to investigate the related mechanism of osteosarcoma by bioinformatics methods. Methods. GSE70367 and GSE69470 were obtained from the GEO database. The differentially expressed genes (DEGs) and miRNAs were analyzed using the GEO2R tool and then visualized with R software. Moreover, the targets of the miRNAs in the DEGs were screened and then used for enrichment analysis. Besides, the STRING database and Cytoscape were applied to illustrate the protein-protein interaction network. RT-qPCR was performed to measure the expression of key genes and miRNAs. Western blot was applied to detect the signaling pathway. Results. 9 upregulated genes and 39 downregulated genes in GSE69470 were identified as the DEGs, and 31 upregulated genes and 56 downregulated genes in GSE70367 were identified as the DEGs. Moreover, 21 common genes were found in the DEGs of GSE70367 and GSE69470. The enrichment analysis showed that the common DEGs of GSE70367 and GSE69470 were related with cell development, covalent chromatin modification, and histone modification and involve in the regulation of MAPK, mTOR, and AMPK pathways. Besides, the miRNAs including miR-543, miR-495-3p, miR-433-3p, miR-381-3p, miR-301a-3p, miR-199b-5p, and miR-125b-5p were identified as the biomarkers of osteosarcoma. In addition, the target genes including HSPA5, PPARG, MAPK14, RAB11A, RAB5A, MAPK8, LEF1, HIF1A, CAV1, GS3KB, FOXO3, IGF1, and NFKBIA were identified as hub nodes. It was found that miR-301a-3p expression was decreased and mRNA expression of RAB5A and NFKBIA was increased in the pathological tissues. The AKT-PI3K-mTOR signaling pathway was activated in pathological tissues. Conclusion. In this study, 7 miRNAs and 13 hub genes were identified, which might be candidate markers. miR-301a-3p, RAB5A, and NFKBIA were abnormally expressed in osteosarcoma tissues.
Objective:To evaluate the clinical effects of lanthanum-contained anti-caries preparation on carious-resistance to the aged root surface,and to furnish evidence for clinical practice.Method:222 the aged patients with gingival marginal atrophy and with root surface exposure were enrolled in study. The patients were randomized into test group and control group.The patients were administered either lanthanum-contained rinse solution in test group or saline solution in control group per day for one month at baseline every year.Clinical measurements of root caries index(RCI) were analyzed at baseline 3 years.Result:The decline in clinical new parameters were significant preferable in test group than in control group.Conclusion:500×10~(-6) mmol/Lanthanum-contained rinse solution per day for one month can leads to significant clinical improvement for root carious-resistance ability,especially suitable for the treatment and prevention of the aged dental root caries.
To study the expression of survivin in ameloblastoma and its clinical significance.Immunohistochemical S-P method was used to detect the expression of survivin in clinical significance. Seventy cases of ameloblastoma (AB), 15 cases of malignant AB and 30 cases of normal oral mucosa were included. SPLUS13.0 software package was used for statistical analysis.Survivin was strongly expressed in AB and malignant AB. The positive rate in malignant AB was up to 100%, followed by 82.9% in AB. Survivin was weakly expressed in normal oral mucosa, with a positive rate of 30%. The difference among the 3 groups was significant (P<0.05).Survivin is overexpressed in AB compared to normal oral mucosa. Survivin is involved in the development and progress of AB, and the ability of invasion and canceration of AB is correlated with the overexpression of survivin.
Birth defects have always been one of the most important diseases in medical research as they affect the quality of the birth population. Orofacial clefts (OFCs) are common birth defects that place a huge burden on families and society. Early screening and prevention of OFCs can promote better natal and prenatal care and help to solve the problem of birth defects. OFCs are the result of genetic and environmental interactions; many genes are involved, but the current research has not clarified the specific pathogenesis. The mouse animal model is commonly used for research into OFCs; common methods of constructing OFC mouse models include transgenic, chemical induction, gene knockout, gene knock-in and conditional gene knockout models. Several main signal pathways are involved in the pathogenesis of OFCs, including the Sonic hedgehog (SHH) and transforming growth factor (TGF)-β pathways. The genes and proteins in each molecular pathway form a complex network to jointly regulate the formation and development of the lip and palate. When one or more genes, proteins or interactions is abnormal, OFCs will form. This paper summarises the mouse models of OFCs formed by different modelling methods, as well as the key pathogenic genes from the SHH and TGF-β pathways, to help to clarify the pathogenesis of OFCs and develop targets for early screening and prevention.
CD47 is a glycoprotein of the immunoglobulin superfamily that is often overexpressed in different types of hematological and solid cancer tumors and plays important role in blocking phagocytosis, increased tumor survival, metastasis and angiogenesis. In the present report, we designed CAR (chimeric antigen receptor)-T cells that bind CD47 antigen. We used ScFv (single chain variable fragment) from mouse CD47 antibody to generate CD47-CAR-T cells for targeting different cancer cell lines. CD47-CAR-T cells effectively killed ovarian, pancreatic and other cancer cells and produced high level of cytokines that correlated with expression of CD47 antigen. In addition, CD47-CAR-T cells significantly blocked BxPC3 pancreatic xenograft tumor growth after intratumoral injection into NSG mice. Moreover, we humanized mouse CD47 ScFv and showed that it effectively bound CD47 antigen. The humanized CD47-CAR-T cells also specifically killed ovarian, pancreatic, and cervical cancer cell lines and produced IL-2 that correlated with expression of CD47. Thus, CD47-CAR-T cells can be used as a novel cellular therapeutic agent for treating different types of cancer.
Rationale: Tumor cells possess sophisticated strategies to circumvent immune detection, including the modulation of endogenous immune checkpoints, particularly those within the B7 family. Elucidating the mechanisms that govern the induction of B7 family molecules is crucial for the advancement of immunotherapy. Lysine lactylation (Kla), a newly identified epigenetic modification, is suggested may play a role in reshaping the tumor microenvironment and facilitating immune evasion. Methods: We analyzed the glycolysis pathway's enrichment in patients with immune-evading tumors and assessed the impact of lactate treatment on the antitumor immunity of CD8+ T cells in the tumor microenvironment. We interrupted glycolysis using lactate dehydrogenase A (LDHA) knockdown and sodium oxamate, and evaluated its effects on CD8+ T cell cytotoxicity. Additionally, we investigated the correlation between B7-H3 expression and the glycolysis pathway, and explored the molecular mechanisms underlying lactate-induced B7-H3 expression. Results: Our findings revealed that the glycolysis pathway was highly enriched in immune-evading tumors. Lactate treatment inhibited the antitumor immunity of CD8+ T cells, whereas interruption of glycolysis via LDHA knockdown or treatment with sodium oxamate augmented the cytotoxicity of CD8+ T cells, effectively counteracting tumor immune evasion. B7-H3 expression was found to be closely linked with the glycolysis pathway. Mechanistically, lactate-upregulated H3K18la directly bound to the B7-H3 promoter in conjunction with the transcription factor Creb1 and its co-activator Ep300, leading to increased B7-H3 expression and contributing to tumor progression by compromising the proportion and cytotoxicity of tumor-infiltrating CD8+ T cells. In mouse tumor bearing models, inhibiting glycolysis and B7-H3 expression suppressed tumor cell growth, activated tumor-infiltrating CD8+ T cells, and demonstrated potent anti-tumor efficacy. Furthermore, this approach enhanced the efficacy of anti-PD-1 treatment. Conclusions: This study uncovers a novel mechanism by which lactate modulates the immune microenvironment through the glycolysis pathway and B7-H3 expression, providing new avenues for lactate metabolism-targeted tumor immunotherapy.
L.monocytogenes is a gram-positive,facultative intracellular bacterium that escapes the phagoly- sosome of host target cells,replicates in the cytosol,and efficiently presents both the class I MHC pathway of endogenous antigen and the classⅡpathway of exogenous antigen.The host's response to L. monocytogenes has been studied for more than 40 years.L.monocytogenes stimulates the innate immune re- sponse to produce cytokines that enhance antigen-presenting function and induce a Th1-type cytokine pro- file associated with cell-mediated immune responses.The natural route of infection by L.monocytogenes is at the mueosa upon oral ingestion,and targeted cells during infection include dendritic cells and macropha- ges.As a vector,foreign genes can be stably inserted into the L.monocytogenes genome and be expressed at high levels into the cytoplasm of host cells for processing and presentation by the major histocompatibility complex classⅠpathway.In this review,the development of methods to transform L.monocytogenes to ex- press and secrete foreign antigens,and the studies that demonstrate genetically engineered L. monocytogenes mutants as highly effective vectors for the induction of potent immune responses against vi- ral antigens and tumor cells were summarized.
Objective To establish a set of scientific,practical and perfect legal system of rural cooperative medical care, and provide a legal basis for the healthy,steady and continual development of the new rural cooperative medical care system. Methods The detailed research and analysis on the development of the new rural cooperative medical care in Anhui province during 2003- 2012 were carried through the investigation and data collection. Results The new rural cooperative medical care system was practiced and developed in the past 10 years. The certain achievements have been made. But there were still some urgent problems to be solved,such as the imperfection of that legal system,the singleness of management mode of that system and the confused supervision for certified hospital,especially the lack of the legal system. Conclusion It is urgent to formulate the legal system of the new rural cooperative medical care.
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