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ObjectiveTo investigate the role and mechanism of DNA repair regulation in the process of hepatocellular carcinoma （HCC） recurrence. MethodsHCC tissue samples were collected from the patients with recurrence within two years or the patients with a good prognosis after 5 years， and the Tandem Mass Tag-labeled quantification proteomic study was used to analyze the differentially expressed proteins enriched in the four pathways of DNA replication， mismatch repair， base excision repair， and nucleotide excision repair， and the regulatory pathways and targets that play a key role in the process of HCC recurrence were analyzed to predict the possible regulatory mechanisms. The independent samples t-test was used for comparison of continuous data between two groups； a one-way analysis of variance was used for comparison between multiple groups， and the least significant difference t-test was used for further comparison between two groups. ResultsFor the eukaryotic replication complex pathway， there were significant reductions in the protein expression levels of MCM2 （P=0.018）， MCM3 （P=0.047）， MCM4 （P=0.014）， MCM5 （P=0.008）， MCM6 （P=0.006）， MCM7 （P=0.007）， PCNA （P=0.019）， RFC4 （P=0.002）， RFC5 （P<0.001）， and LIG1 （P=0.042）； for the nucleotide excision repair pathway， there were significant reductions in the protein expression levels of PCNA （P=0.019）， RFC4 （P=0.002）， RFC5 （P<0.001）， and LIG1 （P=0.042）； for the base excision repair pathway， there were significant reductions in the protein expression levels of PCNA （P=0.019） and LIG1 （P=0.042） in the HCC recurrence group； for the mismatch repair pathway， there were significant reductions in the protein expression levels of MSH2 （P=0.026）， MSH6 （P=0.006）， RFC4 （P=0.002）， RFC5 （P<0.001）， PCNA （P=0.019）， and LIG1 （P=0.042） in recurrent HCC tissue. The differentially expressed proteins were involved in the important components of MCM complex， DNA polymerase complex， ligase LIG1， long patch base shear repair complex （long patch BER）， and DNA mismatch repair protein complex. The clinical sample validation analysis of important differentially expressed proteins regulated by DNA repair showed that except for MCM6 with a trend of reduction， the recurrence group also had significant reductions in the relative protein expression levels of MCM5 （P=0.008）， MCM7 （P=0.007）， RCF4 （P=0.002）， RCF5 （P<0.001）， and MSH6 （P=0.006）. ConclusionThere are significant reductions or deletions of multiple complex protein components in the process of DNA repair during HCC recurrence.
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ObjectiveTo investigate the difference in protein expression between hepatocellular carcinoma (HCC) patients with recurrence and those with good prognosis, the differential expression and regulatory mechanism of miR-152-3p target proteins, and the role of miR-152-3p in the recurrence of HCC. MethodsTMT-labeled proteomic sequencing and RT-PCR were used to measure the expression of proteins and the expression of miR-152-3p in the HCC tissue of six patients with recurrence at 2 years after HCC resection and six patients with good prognosis at 5 years. Six databases were used to analyze the target genes of miR-152-3p, and Gene Ontology, DAVID, and REACTOME databases were used to perform target gene screening, enrichment annotation, and signal transduction pathway enrichment analysis. Gene mutation frequency and survival curve analysis were performed for the target genes of miR-152-3p to verify the role of miR-152-3p target genes in patients with HCC recurrence. The independent samples t-test was used for comparison of continuous data between two groups, and a Kaplan-Meier analysis was performed to investigate the survival rates of liver-related genes. ResultsCompared with the patients with HCC recurrence, the patients with good prognosis after HCC resection had a significantly higher transcriptional expression level of miR-152-3p in HCC tissue (P＜0.05). The results of protein sequencing showed that there were 365 differentially expressed proteins in HCC tissue between the patients with good prognosis and the patients with recurrence, and the analysis of HCC recurrence databases showed that 17 proteins were regulated by miR-152-3p. Further analysis of the signaling pathways showed that the function of the 17 target genes regulated by miR-152-3p was enriched in the translation and regulation of mitochondria and ribosome, and multiple enrichment revealed that six target genes were closely associated with mitochondrial respiratory chain complex, i.e., AKAP1, FOXRED1, MRPL28, MRPL50, SHC1, and STAU1. Gene mutation frequency and survival curve analysis showed that the loss or weakening of the function of mitochondrial respiratory chain-related target proteins seriously affected the prognosis and survival rate of patients. ConclusionThere is a significant difference in the expression of miR-152-3p in HCC tissue between patients with good prognosis and those with recurrence after HCC resection, and miR-152-3p may lead to the recurrence of HCC by regulating the target genes AKAP1, FOXRED1, MRPL28, MRPL50, SHC1, and STAU1, acting on the mitochondrial respiratory chain, and affecting the oxidative respiratory function of cells.
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Objective To observe the curative effect of low molecular heparin for treating secondary high coagulation state in the patients with nephrotic syndrome(NS) .Methods Total 87 cases of NS in our hospital were divided into the conventional treat‐ment group (n=42) and the low molecular heparin treatment group (n=45) .The routine treatment group was given the prednisone treatment and the low molecular heparin treatment group was treated by low molecular heparin combined with prednisone .The re‐lated indicators of blood coagulation before and after treatment were detected and the clinical curative effects in two groups were an‐alyzed .Results The coagulation related indicators in the conventional treatment group had no statistically significant difference be‐tween before and after treatment (P>0 .05) ,the prothrombin time(PT) and activated partial thrombin time(APTT) after treat‐ment in the low molecular heparin treatment group were significantly extended compared with before treatment ,while the concen‐trations of D‐dimer and fibrinogen were significantly decreased and the concentration of antithrombin Ⅲ was markedly increased compared with before treatment ,showing statistically significant differences between the two groups (P<0 .05);the patients of the low molecular heparin group patients had no bleeding after treatment .Conclusion Low molecular heparin combined with predni‐sone can reduce the secondary high condensation state in NS without bleeding and has a significantly clinical effect .
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Objective To study the effects of taking clopidogrel on relevant indicators of platelet aggregation function in 138 cases acute coronary syndrome (ACS) .Methods The platelet function analyzer and flow cytometry were adopted to detect the ADP‐induced platelet aggregation rate ,P selectin and activated GP Ⅱ b/ Ⅲ before medication and on 7 d after taking clopidogrel . Results The platelet aggregation rate after taking clopidogrel for 7 continuous d was decreased significantly (P<0 .01);the P se‐lectin level and activated GP Ⅱ b/ Ⅲ a expressed on platelet surface were significantly reduced (P<0 .01) as well .Conclusion Taking clopidogrel could reduce the platelet aggregation significantly in the patients with ACS and has the effect for inhibiting the platelet aggregation .
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Objective To analyze the expression of T lymphocyte activation antigen in peripheral blood of aged patients with non-small cell lung cancer . Methods The lymphocytes from peripheral blood in 45 aged patients with non-small cell lung cancer were immunologically labeled in double fluorescence and CD3-FITC, CD25/HLA-DR and CD69-PE and determined by flow cytometry. Normal aged donors, young patiens with lung cancer and aged benign lesion group were used as controls. Results Peripheral blood CD3 +/CD25 +, CD3 +/HLA -DR + and CD3 +/CD69 + in T lymphocyte with 45 aged lung cancer(7.24?1.85,28.46?5.39 and 7.78?2.63, respectively) were significantly lower than those in normal aged controls(10.35?2.54,37.16?5.51,11.02?2.18, respectively)and aged benign lesion (9.53?3.02, 35.33?5.23, 10.67?2.45, respectively)( P 0.05). Significant differences were found among them in stages Ⅲ, Ⅳ(7.15?1.13, 25.32?5.23, 7.14?2.81, respectively) and stagesⅠ,Ⅱ(8.06?1.21, 30.27?6.05, 8.43?2.67, respectively)( P 0.05). Conclusions Detection of CD3 +/CD25 +, CD3 +/HLA -DR + and CD3 +/CD69 + levels by flow cytometry might be helpful for reflecting the human immune function and the prognosis evaluation in patients with aged non-small cell lung cancer.
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<p><b>BACKGROUND</b>To investigate the expression feature of Cx43 protein in non-small cell lung cancer and its clinical significance.</p><p><b>METHODS</b>Paraffin embedded tissues from 65 patients with primary non-small cell lung cancer and 20 adjacent non-cancerous lung tissues were investigated for expression of Cx43 protein by immunohistochemistry (ABC method). The relationship between Cx43 protein expression and clinicopathological characteristics of lung cancer was analyzed.</p><p><b>RESULTS</b>Cx43 protein was positively expressed in 24 out of 65 lung cancer tissues (36.92%), and in all 20 adjacent non-cancerous lung tissues. There was a significant difference in Cx43 expression between stage I-II and stage III-IV groups ( P < 0.05), as well as between moderate-well and poor differentiation groups ( P < 0.01). Primary lung cancer tissues with lymph node metastasis showed lower expression of Cx43 than those without lymph node metastasis ( P < 0.01). The positive rate of Cx43 expression was not related to histological classification ( P > 0.05).</p><p><b>CONCLUSIONS</b>Cx43 expression might play a role in the genesis, development and metastasis of lung cancer. It may be used to judge the biological behavior of lung cancer.</p>