Objective To explore the clinical value of combined detection of lysophosphatidic acid(LPA),tumor-specific growth factor(TSGF)and carbohydrate antigen 1 9-9(CA1 9-9)in the diagnosis of non-small cell lung cancer(NSCLC).Methods The ser-um levels of LPA,TSGF and CA1 9-9 in 97 cases of patients with NSCLC(NSCLC group),43 cases of patients with benign lung disease(benign lung disease group)and 50 cases of healthy individuals(healthy control group)were detected,and diagnostic value of combined detection of these three tumor makers in the diagnosis of NSCLC was analysed.Results Serum levels of LPA,TSGF and CA1 9-9 in the NSCLC group were significantly higher than those in the benign lung disease group and healthy control group,had statistically significant differences(P <0.05).The sensitivity and specificity of combined detection of LPA,TSGF and CA1 9-9 was 68.63% and 37.1 7% respectively,and the sensitivity was higher than that of single detection and combined detection of any two of the three indicators.Conclusion Combined detection of tumor markers can improve the sensitivity in the diagnosis of NSCLC, which could provide reliable laboratory references for diagnosing NSCLC.

Objective To detect the expressions of two protein factors hypoxia-inducible factor (HIF)-1α and Helicobacter pylori (Hp) in gastric cancer in Mongolian and Han two nationalities respectively,and to explore the relationship of HIF-1α and Hp in the development of gastric cancer.Methods A modified Warthin-Starry (W-S) silver staining method was used to detect Hp infection in 27 Mongolian patients with gastric cancer and 30 Han patients with gastric cancer.Immunohistochemical (S-P) method and reverse transcription polymerase chain reaction (RT-PCR) method were used to detect protein and mRNA expressions of HIF-1α in cancer tissue,paracancerous tissue and normal tissue samples.The relationship of HIF-1α protein and Hp expression was analyzed between gastric carcinoma tissue samples of Mongolian patient group and Han patient group.Results Hp infection rates were 81.5％ (22/27) and 66.7％ (20/30) in Mongolian and Han patients with gastric cancer.The difference in infection rate was not statistically significant between two groups of patients (~=1.608,P ＞ 0.05).The positive expression levels of HIF-1α protein were 62.96％ (17/27) and 70.00％ (21/30) in gastric cancer tissue samples of Mongolian and Han groups.The relative expression levels of HIF-1α mRNA were 0.891 4±0.075 0 and 0.907 4±0.065 5.There was no significant difference in the HIF-1 α mRNA expression between the two nationalities.No positive expressions of HIF-1α protein and mRNA were found in paracancerous tissue and normal tissue samples.There was a positive correlation in the positive expression of HIF-1α protein and Hp infection in gastric cancer tissue samples of Mongolian and Han patient groups (r,=0.424 and 0.617,P ＜ 0.05).Conclusion HIF-1α and Hp are pathogenic factors of gastric cancer.Hp and HIF-1α may promote the occurrence of gastric cancer together.The pathogenic mechanism of HIF-1α and Hp in gastric cancer may be the same for Mongolian and Han patients.

Fifteen patients with spasticity were treated by phenol blocks. The results are satisfactory.Phenol blocks has the advantages of high selectivity,few side-effects and low cost. The anthor recommends that phenol blocks could be used in clinical antispasticity treatment.

Recently, there has been a growing focus on investigating the influence of periodontitis on the aging population. There is epidemiological evidence that indicates periodontitis is associated with mortality, and it has been shown to accelerate the biological processes of aging. However, the precise mechanism by which periodontitis accelerates the process of the aging population remains to be elucidated. This paper reviews relevant research results and finds that periodontitis may be associated with accelerated aging and increased mortality through the following mechanisms: 1) the inflammatory mediators produced by periodontitis are released into the bloodstream and promote “inflammageing”, which accelerates aging through activation of the NF-κB signaling pathway and the senescence-associated secretory phenotype; 2) periodontal pathogens can promote the aging process in the following three ways: ① periodontal pathogens and bacterial products promote “inflammageing” through blood circulation, and they lead to abnormal changes in SIRT1 and mTOR, important aging markers in the blood, which induces mitochondrial dysfunction and accelerates aging; ② porphyromonas gingivalis overactivates the Akt/FoxO1 pathway to directly promote the aging of dendritic cells and produce exosomes that transmit and amplify paracrine immunosenescence; and ③ periodontal pathogens are ectopically colonized in the intestinal tract and lead to gut dysbiosis, thus indirectly accelerating the aging process.