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Objective:To investigate the expression of microRNA-324-5p (miR-324-5p) and transcription factor forkhead box C1 (FOXC1) in glioma and their relationship with the prognosis of patients.Methods:From March 2012 to March 2015, a total of 72 cases of glioma tissues were collected from glioma patients who were admitted to Chongqing Hygeia Tumor Hospital and the People's Hospital of Nanchuan in Chongqing, and 28 cases of normal human brain tissues resected in craniocerebral surgery were also collected. The expressions of miR-324-5p and FOXC1 mRNA were detected by real-time fluorescent quantitative polymerase chain reaction (qRT-PCR), and the expression of FOXC1 protein was detected by immunohistochemistry. Pearson method was used to analyze the correlation between the expressions of miR-324-5p and FOXC1 in glioma tissues; Kaplan-Meier method was used to analyze the survival of patients with glioma; Cox regression analysis was used to analyze the risk factors affecting the prognosis of patients with glioma.Results:FOXC1 protein was mainly located in the cytoplasm of glioma, and its positive expression rate in glioma tissues was 81.94% (59/72), which was significantly higher than that in normal brain tissues [17.86% (5/28)], and the difference was statistically significant ( χ2 = 35.938, P<0.01). Compared with normal brain tissues, the expression of miR-324-5p was down-regulated in glioma tissues (0.62±0.19 vs. 0.98±0.02, t = 9.974, P < 0.05), and the expression of FOXC1 mRNA was up-regulated (1.41±0.29 vs. 0.99±0.02, t = 7.633, P < 0.05). The expressions of miR-324-5p and FOXC1 protein were correlated with the number of primary lesions, differentiation degree, TNM stage and lymph node metastasis of glioma (all P<0.05). Pearson analysis showed that the expressions of miR-324-5p and FOXC1 mRNA were negatively correlated ( r = -0.550, P<0.01). The 5-year overall survival rate of patients in miR-324-5p high-expression group was significantly higher than that of patients in miR-324-5p low-expression group (45.71% vs. 24.33%, χ2 = 6.531, P = 0.011), and the 5-year overall survival rate of patients in FOXC1 protein high-expression group was significantly lower than that of patients in FOXC1 protein low-expression group (30.41% vs. 42.34%, χ2 = 3.631, P = 0.047). Multivariate Cox regression analysis showed that low differentiation, TNM stage Ⅲ-Ⅳ, lymph node metastasis, low expression of miR-324-5p and high expression of FOXC1 protein were independent risk factors for prognosis of glioma patients (all P < 0.05). Conclusions:The expression of miR-324-5p is low and the expression of FOXC1 is high in glioma. They may be involved in the regulation of tumor differentiation and metastasis, and related to the poor prognosis of patients. They may be potential therapeutic targets for glioma.
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Objective To retrospectively analyze the platelet count and related factors in bleeding patients with hematonosis,and to calculate the risk of bleeding when the platelet count is at each exposure level.Methods Retrospective analysis of patients from Department of Hematology Inpatients in Nanjing Drum Tower Hospital,Nanjing First Hospital and Nanjing Jiangning Hospital from July 2013 to June 2017 was collected.And the risk of bleeding for different hematonosis was calculated.Results The tolerance of the 5 categories of hematonosis to low platelet counts is compared:AA and ITP can tolerate lower levels of platelet count;MDS and AML(except M3) are more prone to bleeding;ALL is the most susceptible to bleeding.Conclusion When platelet resources are scarce,priority should be given to ALL,MDS and AML patients,in order to ensure the safety of critically ill patients.For patients with AA and ITP,the platelet infusion threshold may be reduced appropriately,in oder to reduce the incidence of platelet transfusion refractoriness.
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Juvenile hemochromatosis is an autosomal recessive disease characterized by progressive tissue iron overload which leads to irreversible organ damage and even death.This disease is mainly caused by mutations in two genes:hemojuvelin gene and hepcidin gene.Different mutations have different phenotype.The two genes may act as modifying genes in HFE hemochromatosis.Hepcidin secreted by liver plays a central role in the regulation of iron homeostasis.HJV can act as a bone morphogenetic protein(BMP)co-receptor which is required for HJV to regulate hepcidin expression and iron homeostasis.Recent researches suggest that the bone morphogenetic protein(BMP)signaling pathway mediated by HJV is a significant mechanism for HJV to regulate hepcidin expression and iron homeostasis.HJV mutant impaires BMP signaling which results in hepcidin expression decrease and abnormal iron metabolism.
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Objective To explore the expression and significance of CD34, CD117 on bone marrow mononuclear cells of myelodysplastic syndromes (MDS). Methods Direct immunofluorescence staining was used by means of flow cytometry. 37 patients with MDS were divided into RA/RARS/RCMD subgroup, RAEB Ⅰ/RAEB Ⅱ subgroup; favorable chromosomal subgroup, poor chromosomal subgroup; intermediate-risk Ⅰ subgroup, intermediate-risk Ⅱ subgroup, high-risk subgroup respectively according to WHO classification,cytogenetic abnormalities and international prognostic scoring system (IPSS). Results CD34 and CD117 were positive respectively in 11 of 19 patients with RMRARS/RCMD, all cases in RAEB Ⅰ/RAEB Ⅱ expressed CD34 and CD117; increased expression of CD34 and CD117 was MDS grade-related. Favorable chromosomal subgroup, 14 of 22 patients were positive for CD34, CD117, all cases in poor chromosomes expressed CD34 and CD117; there was a direct relationship between phenotytic density and poor cytogenetic risk factor. CD34 and CD117 expression was present respectively in intermediate-risk Ⅰ (9/17), intermediate-risk Ⅱ (11/11) and highrisk subgroup (9/9); the phenotypic intensity also was correlated with IPSS scores. Conclusion Detection of CD34, CD117 may be a useful tool for subtyping and predicting the prognosis of MDS.
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Objective To examine the frequency and the course of cytomegalovims infection after allogeneic hematopoietic stem cell transplantation, and correlation of transplant factors with Cytomegalovirus (CMV) infection and viral load. Methods Using real-time polymerase chain reaction, we detected the copies of CMV-DNA in blood samples of the 62 patients after allo-HSCT. Furthermore, we studied the relationship between transplant factors and CMV infection. Results Among the total, 23 cases were contracted with CMV infection, 4 cases developed to CMV disease. 22 cases were cured and 1 case died. Course of CMV infection influenced the viral load significantly. Donor type, stem cell source, use of ATG, Ⅱ-Ⅳ grade aGVHD, use of glucocorticoid, complicating with other infection and use of cellular filter significantly influenced CMV infection. However, in multivariate analysis, none of them was the independent risk factors. Conclusion Real-time polymerase chain reaction may be used to early diagnose of the CMV infection and to guide treatment. Many factors influenced CMV infection. Early diagnosis and treatment could decrease the morbidity and mortality of CMV infection.
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<p><b>OBJECTIVE</b>To analyze the phenotype and genotype of a family with inherited dysfibrinogenemia.</p><p><b>METHODS</b>Laboratory tests including activated particle thromboplastin time (APTT), prothrombin time (PT), thrombin time (TT), and the activity of protein C (PC), protein S(PS) and antithrombin (AT) were conducted in the proband and 4 family members. The activity and antigen of fibrinogen in plasma were measured by functional and immunoturbidimetry assay, respectively. All the exons and exon-intron boundaries of the three fibrinogen genes were analyzed by direct sequencing.</p><p><b>RESULTS</b>The proband had normal APTT and PT, but prolonged TT. Her plasma fibrinogen levels were extremely reduced, which was also found in her mother. The sequencing results of the proband revealed heterozygous g.5678 G>A in the exon 8 of FGG gene originating from her mother, which caused Arg275His missense mutation.</p><p><b>CONCLUSION</b>Dysfibrinogenemia in the family is caused by Arg275His in the beta chain of fibrinogen and it is the first report on a Chinese family with inherited dysfibrinogenemia.</p>