Objective To investigate the single nucleotide polymorphisms (SNPs) at codons 16 and 27 of β2-AR gene in pancreatic carcinoma and non-neoplastic pancreatic tissues,and the correlations between these SNPs and the expression of β2-AR protein in pancreatic carcinoma.Methods A total of 64 cases of pancreatic carcinoma (PC) and 20 non-neoplastic pancreatic tissues (NPC) were genotyped at codons 16 and 27 by PCR-restriction fragment length polymorphism (PCR-RFLP) and DNA sequencing.The correlations between the distribution of genotypes and clinicopathological characteristics of pancreatic carcinoma were analyzed.The expression of β2-AR protein was detected by immunohistochemistry in pancreatic carcinoma.Results The distributions of genotype frequency at codons 16 and 27 in PC and NPC were in accordance with the Hardy-Weinbery equeilibrium.The frequencies of their genotypes (AA,AG and GG) and frequencies of alleles A and G at codon 16 between PC and NPC showed no difference.The genotype frequencies were associated with TNM grade,lymph node metastasis,one-year survival rate (P=0.03,0.05,0.04),but they were not associated with patients' gender,age,histological differentiation and size of tumor.The allele G at codon 16 was frequently appeared in tumors with high TNM grade,lymph node metastasis,low one-year survival rate (P＝ 0.01,0.03,0.02),and high expressions of β2-AR protein (P =0.02).The frequencies of two genotypes (CC and CG) and frequencies of alleles C and G at codon 27 showed no difference between PC and NPC.The genotype frequencies and allele frequencies of codon 27 were not associated with patients' clinicopathological features,and expressions of β2-AR protein.Conclusions SNPs of β2-AR gene were associated with biological behaviors of pancreatic carcinoma.Allele G at codon 16 was associated with high risks of lymph node metastasis,high TNM grade,low one-year survival rate,and high expressions of β2-AR protein.Allele G at codon 16 might facilitate the progression and metastasis of pancreatic carcinoma through elevating the expression of β2-AR.SNPs at codon 16 of β2-AR are new useful biomarkers for predicting biological behaviors and survival of pancreatic carcinoma and might be used as a new gene therapeutic target.

3 cm in diameter was 65.6%, while the rate in those

Though Runx2 and Osterix are both key transcription factors in the pathway of osteoblast differentiation, whether Runx2 positively regulates Osterix being unknown. It was showed that Runx2 induced the gene expression of Osterix both in the non-osteoblastic cell lines, either pluripotent or differentiated, and in the osteoblastic cell lines. At the same time, the results also indicated that Runx2 up-regulated the activity of the 3.2 kb human Osterix promoter. Further experiments identified a highly conserved and functional Runx2 binding site "AGTGGTT" within the promoter. Thus the results support the hypothesis that Runx2 is involved in the regulation of the Osterix gene expression. Moreover, the transient transfection and dual-luciferase assay showed Osterix up-regulated the activity of the 2.3 kb type Ⅰ collagen promoter in the non-osteoblastic cells, but Runx2 did not. This difference implies that Osterix, the down stream transcription factor of Runx2 during osteoblast differentiation, is needed to stimulate the osteoblast-specific gene expression of type Ⅰ collagen.

Objective To explore effect of 5 -aminolevulinic acid -photodynamic therapy combined with thymopentin -5 on IL -17,IL -23 expression of recurrent condylomata acuminata patients.Methods 140 patients with recurrent condylomata acuminata were randomly divided into 3 groups.53 cases in observation group were treated by 5 -aminolevulinic acid -photodynamic therapy combined with thymopentin -5,42 cases in control group 1 were treated by 5 -aminolevulinic acid -photodynamic therapy,and 45 cases in control group 2 were treated by thymopen-tin -5.24 healthy subjects were served as normal controls.IL -17,IL -23 levels were determined by enzyme linked immunosorbent assay before and after the clinical therapy.Results IL -17,IL -23 levels in the patients with recur-rent condylomata acuminata were significantly lower than those in healthy subjects(t =28.10,P <0.01;t =11.10, P <0.01).There were significant differences in IL -17,IL -23 between recurrent condylomata acuminata patients and healthy persons before treatment.There was significant difference after treatment(t =61.17,P <0.01;t =28.02, P <0.01).Conclusion 5 -aminolevulinic acid -photodynamic therapy combined with thymopentin -5 in the treat-ment of recurrent condylomata acuminata inhibited IL -17,IL -23 expression,so as to achieve therapeutic effect.

Objective To investigate serum total IgE levels of healthy population in two hospitals in Yantai and Weihai areas,to investigate the influencing factors of the levels of serum total IgE,which can provide information for the clinical diagnosis of allergic diseases.Methods The total serum IgE level was measured with chemiluminescence method in 1 200 cases of healthy people and 600 cases of smoking group in different age groups.Results The total IgE level of ≤6 years was (28.53±20.71)IU/mL,7-12 years was (29.74±25.94)IU/mL,13-18 years was (32±22.32)IU/mL,19-44 years was (45.2±36.27)IU/mL,45-60 years was (35.47±27.23)IU/mL,>60 years was (31.2±25.03)IU/mL.There was no effect of serum total IgE in different age groups:≤6 years,7-12 years,13-18 years,45-60 years,>60 years(t=0.610,1.508,0.777,0.160,1.518,all P>0.05),19-44 years was significantly different from other age groups(t=0.075,P<0.01).There was no gender difference of serum total IgE in different age groups (P>0.05).The total IgE level of the smoking group:19-44 years was (55.22±39.16)IU/mL,45-60 years was (42.63±28.46)IU/mL,>60 years was (39.32±26.73)IU/mL.The level of serum IgE in the smoking group was significantly higher than that in the same age group (t=0.142,0.174,0.235,all P<0.05).Conclusion No significant difference existed in healthy people of serum total IgE levels from birth to adulthood.However,the total IgE level rose when reached to 19-44 years,which then slightly declined as the growth of the age.There was no significant difference between male and female of the IgE levels in different age groups.But after the age of 19,smoking can lead to the increase of the total IgE level.

Objective　 To investigate gene rearrangement and p53 expression i n defining the nature of angioimmunoblastic lymphadenopathy. Methods　 DNA was ext racted from paraffin-embedded tissue blocks of 44 angioimmunoblastic lymphaden o pathy (AIL) patients and analyzed with polymerase chain reaction (PCR) for IgH and TCRγ gene rearrangement. Immunohistochemistry staining was used to detect p53 protein expression. Thirty-five cases were followed-up. Results　 12 out of 44 cases(27.3%) showed TCRγ gene rearr angement and 2 (4.5%) showed IgH gene rearrangement. Rearrangement of both IgH a nd TCRγ genes were detected in 2 cases(4.5%). 14 cases (31.8%) showed p53 posit i ve expression, among which 12 showed positive rearrangement and 2 showed negative (P<0.01). Eight out of 11 patients of p os itive gene rearrangement died in one year, while only 3 patients were still aliv e at the eighteenth month of follow-up, three of 24 patients of negative gene r earrangement were found dead at the time of the one year follow-up, while the r est 21 patients were alive and the longest survival time was 96 months. Conclusions　 Gene rearrangement can define th e pathological nature of AIL. The expression of p53 is highly related to gene r earrangement, and thus an important immunological marker in research on AIL.

Objectives: . Nicotine is an ingredient of tobacco, and exposure to nicotine increases the risks of various cancers, including oral cancer. Previous studies have focused on the addictive properties of nicotine, but its carcinogenic mechanism has rarely been studied. We aimed to explore the key genes in the process through which nicotine promotes the occurrence and development of oral cancer via data mining and experimental verification. Methods: . This study involved three parts. First, key genes related to nicotine-related oral cancer were screened through data mining; second, the expression and clinical significance of a key gene in oral cancer tissues were verified by bioinformatics. Finally, the expression and clinical significance of the key gene in oral cancer were histologically investigated, and the effects of its expression on cell proliferation, invasion, and drug resistance were cytologically assessed. Results: . SERPINE1 was identified as the key gene, which was upregulated in nicotine-treated oral cells and may be an independent prognostic factor for oral cancer. SERPINE1 was enriched in various pathways, such as the tumor necrosis factor and apelin pathways, and was related to the infiltration of macrophages, CD4+T cells, and CD8+T cells. Overexpression of SERPINE1 was associated with N staging and may be involved in hypoxia, angiogenesis, and metastasis. Knockdown of SERPINE1 in oral cancer cells resulted in weakened cell proliferation and invasion ability and increased sensitivity to bleomycin and docetaxel. Conclusion . This study revealed SERPINE1 as a key gene for nicotine-related oral cancer, indicating that SERPINE1 may be a novel prognostic indicator and therapeutic target for oral carcinoma.