Objective To investigate and compare PM2.5pollution levels in Taiyuan and Beijing and to study the DNA damage induced by PM2.5.Methods PM2.5pollution levels in Taiyuan with coal smoke pollution and in Beijing with mixing air pollution typed by coal smoke and automobil exhaust were monitored,and the DNA damage induced by PM2.5was detected by single cell gel-electrophoresis(SCGE)(Comet assay)using human alveolar epithelial cell line A549(A549cells).Results The PM2.5pollution levels in Taiyuan and Beijing during winter were0.132-0.681mg /m 3 and0.028-0.436mg /m 3 respective-ly.PM2.5could induce DNA damage in A549cells after exposure to doses of5,50and200?g /ml for12h and24h-incuba-tion.Compared with the negative control group,there were significant differences(P

OBJECTIVE:To study whether there is interaction between ambroxol hydrochloride and amino?phylline.METHODS:16volunteer were randomly divided into trial group and control group.The blood concentration of amin_ ophylline was determinated with HPLC method,then the main parameters of pharmacokinetics of aminophylline were calculated with3p97software.RESULTS:The main parameters of pharmacokinetics of aminophylline in trial and control group were:K e (0.062?0.023)/h and(0.0905?0.013)/h;V(22.83?7.85)and(23.27?3.78)L;T 1/2 (12.51?4.2)and(7.77?0.89)h;AUC 0～21 (426.59?186.92)and(245.74?48.6)(mg?h)/L;CL(s)(23.17?9.83)and(34.84?6.00)ml/min respective?ly.CONCLUSION:Although ambroxol hydrochloride did not influence the distribution of aminophylline,but it could prolong the half time of aminophylline and increase the stagnation time of aminophylline in vivo.

AIM: To investigate the effect of extracellular signal-regulated kinase 1/2 signaling pathway after severe diffuse brain injury (DBI) in rats, and to provide base for treatment. METHODS: Male Sprague-Dawley rats were randomly divided into four groups: control group, traumatic group, low dose of inhibitor U0126 treatment group and high dose of inhibitor U0126 treatment group. DBI rat model was established according to the description of Marmarou's diffused brain injury. At 30 min and 1 h, 6 h, 24 h, 48 h and 72 h after injury, morphological changes were observed under light and electronic microscopes. The ERK1/2 phosphorylation and c-Fos were measured by Western blotting. Apoptosis was measured with TUNEL method. Learning and memory function were performed with Morris water maze from 3 days to 7 days after injury. RESULTS: After trauma, some neurons displayed histopathologic changes of necrosis and apoptosis, axon myelin sheath internalization and disconnection. ERK1/2 phosphorylation protein was apparently increased at 30 min after injury, approached peak at 6 h and continued to 24 h. c-fos protein was markedly increased at 30 min after injury, approached peak at 6 h and returned to bottom at 24 h. The number of apoptotic nerve cells increased at 6 h after and approached peak at 72 h. Latencies of searching safety island prolonged. Rats treated with U0126 had reduction in ERK1/2 activity, c-Fos protein, neuronal apoptosis and searching safety island latencies. CONCLUSION: The activated ERK1/2 signaling pathway plays an important role in processing of nerve cell apoptosis after severe DBI.

Objective To study the role of human MutS homolog 2 (hMSH2), a newly identified protein ligand that was recognized by Vγ9δ2 T cells , in innate anti-gastric carcinoma immunity .Methods Flow cytometry and laser confocal microscopy were used to identify hMSH 2 that ectopically expressed on gas-tric carcinoma cell line 803.An anti-hMSH2 antibody was used to block hMSH2 to evaluate its effects on the cytotoxicity of Vγ9δ2 T cells and their cytokines secretion .Subcellular distribution of hMSH 2 in gastric car-cinoma tissues was examined by tissue microarray immunohistochemistry analysis .Results Ectopic mem-brane expression of hMSH 2 was observed on 803 cells at a relatively high level .Vγ9δ2 T cells blocked with specific anti-hMSH2 antibody showed a decreased cytotoxicity and a reduced IFN-γbut an increased TNF-αsecretion.Ectopic expression of hMSH2 was found in various types of gastric carcinoma tissues at different stages.Enhanced expression of hMSH2 was detected in specimens collected from patients with chronic super-ficial gastritis.Conclusion Ectopically expressed hMSH2 served as a stress-induced endogenous ligand which could promote the cytotoxicity of Vγ9δ2 T cells against gastric carcinoma cells and enhance their IFN-γsecretion.hMSH2 played an essential role in innate anti-gastric carcinoma immunity .

Objective To observe safety and efficacy of intrauterine device MYCu IUD that releases indomethacin. Methods In total, 2000 women requiring IUD for contraception were chosen from domestic multiple clinical centers according to an unified standard. MYCu IUD and TCu380A IUD were randomly inserted for 1000 women each, respectively. All women were regularly followed-up one, three, six and 12 months after insertion. Results All the women were followed-up for 11 985.9 and 11 753.6 person-months in MYCu IUD and TCu380A IUD groups, respectively, with cumulative IUD application rates of 97. 80% and 94. 70%, and cumulative pregnancy rates with IUD of 0. 10% and 0. 31%, respectively. Cumulative expulsion (or partial expulsion) rate in MYCu IUD group was 0. 10%, significantly lower than that in TCu380A IUD one (1.73%), P ＜0. 01, and cumulative removal rate due to medical reasons (bleeding or pain) was 1.51 % and 2. 94%, respectively, P ＜ 0. 05. Rate of IUD-associated termination and overall rate of termination differed significantly between the two groups, P ＜0. 01. Adverse reactions one, three, six and twelve months after IUD insertion included irregular bleeding, prolonged menstruation, increased menstrual blood volume and pain, less in indomethacin-containing MYCu IUD group than those in TCu380A IUD without containing it, P ＜ 0. 01. Conclusions MYCu IUD is a comparatively ideal IUD that should be promoted for extensive use, with extremely low expulsion rate, good contraceptive effect, convenience and safety in insertion and removal, and less adverse effects.

Objeetive To analyze the clinical efficacy of liver transplantation (OLT) for patients with hepatopulmonary syndrome (HPS).Methods From 2008 to 2013,420 adult patients underwent liver transplantation in our hospital.There were 91 patients with,and 329 patients without,HPS.The 5-year survival and mortality rates after OLT for the two groups were retrospectively analyzed.Results There were no significant differences between patients without and with HPS in age,primary disease,Child-Pugh score,MELD score,cold ischemia time and warm ischemia time.However,the differences on serum albumin [(29.6 ± 1.2) g/L vs.(26.4 ± 1.6) g/L] and blood oxygen pressure [(61.0 ±9.0) mmHg (1 mmHg =0.133 kPa) vs.(87.0 ± 6.0) mmHg] were significantly different (P ＜ 0.05).The 1-year cure rate was 65.9％ (60/91) in 91 patients with HPS after liver transplantation.The 1,3,5-year cumulative survival rates for patients without HPS were 97.3％,90.9％ and 80.3％,respectively,and the main causes of death were primary graft dysfunction,recurrent cardiovascular events and primary disease recurrence or tumors.The 1,3,5-year cumulative survival rates for patients with HPS were 65.9％,59.3％ and 56.0％,and the main causes of death were multiple-organ failure,pulmonary infection and cerebrovascular events.Kaplan-Meier survival curve analysis showed that the survival of patients with HPS was significantly lower than that of patients without HPS (P ＜ 0.05).Conclusions Liver transplantation is the most effective treatment for patients with HPS,but the short-term mortality rate is relatively high.We still need to learn more about HPS to improve the survival rate of patients with HPS after liver transplantation.

OBJECTIVE: To evaluate the role of human calcium-activated chloride channel 1 (hCLCA1) and mucin MUC5AC in allergic rhinitis. METHOD: The expression of hCLCA1 and MUC5AC were determined by RT-PCR and immunohistochemical assay in nasal mucosa on 20 patients with allergic rhinitis and 7 normal persons. RESULT: The expression of hCLCA1mRNA in allergic rhinitis group was positive, whereas in normal control group was absent (P<0.01). The expression of MUC5AC mRNA and MUC5AC protein in the allergic rhinitis group were higher than that in the control, respectively (both P<0.01). The increased expression of hCLCA1mRNA in allergic rhinitis group were well correlated with the expression of MUC5ACmRNA and MUC5AC protein and the correlation coefficients were 0.752 and 0.694(both P<0.05). CONCLUSION Upregulation of hCLCA1 mRNA expression may play a pivotal role in mucus overproduction in allergic rhinitis group. The inhibition of HCLCA1 expression may provide a new strategy for the treatment of allergic rhinitis.
Adolescent ; Adult ; Chloride Channels ; metabolism ; Female ; Humans ; Male ; Middle Aged ; Mucin 5AC ; metabolism ; Nasal Mucosa ; metabolism ; Rhinitis, Allergic, Perennial ; metabolism ; Young Adult

Extracellular 5'-nucleotidase (CD73) is not only highly expressed in a variety of solid tumor tissues, but also closely related to tumor stage, treatment and tumor prognosis. CD73 can exert a wide range of immunosuppressive effects through multiple pathways such as A2A receptor, regulation of regulatory T cells, and inhibition of inflammation. Blocking CD73 molecules can not only effectively activate anti-tumor immune responses, but also significantly improve the clinical efficacy of programmed death 1 (PD-1)/programmed death ligand 1 (PD-L1) antibodies. Thus, CD73, as a new immunological checkpoint molecule in the tumor microenvironment, may become a promising new immunotherapy target following CTLA4, PD-1/PD-L1.

Objective: To study the associations between variants of mTORC1 of PI3K/AKT/mTOR pathway and colorectal cancer. Methods: In this hospital-based case-control study, at the First Affiliated Hospital, Xinjiang Medical University from 2000 to 2013, 665 primary colorectal cancer cases and 695 cancer-free controls were genotyped at 10 potentially functional single nucleotide polymorphism (SNPs) loci of mTORC1 (mTOR: rs1034528, rs2295080; Raptor: rs1062935, rs3751934; mLST8: rs3160, rs26865; DEPTOR: rs2271900, rs4871827; AKT1S1: rs2290774, rs2353005) to assess their associations with risk of colorectal cancer by Logistic regression analysis. Results: In single-locus analysis, found a significantly decreased risk of colorectal cancer associated with mLST8 rs26865 by recessive genetic model, especially in populations of ≤68 years of age (OR=0.64; 95%CI=0.43-0.96, P=0.031), female (OR=0.61; 95%CI=0.38-0.99, P=0.046), non-smoking (OR=0.55; 95%CI=0.35-0.87, P=0.010). mTOR rs1034528 CC genotypes were associated with higher risk of colorectal cancer in >68-year-old populations (OR=3.34; 95%CI=1.12-9.91, P=0.030). Raptor rs3751934 CA/AA genotypes were associated with lower colorectal cancer risk in population of body mass index(BMI)>25 kg/m² (OR=0.68; 95%CI=0.47-0.98, P=0.038); and AKT1S1 rs2290774 CC genotypes were associated with lower colorectal cancer risk in non-smoking population (OR=0.67; 95%CI=0.45-0.99, P=0.048). Furthermore, found that populations carrying more than two low-risk genotypes were associated with lower colorectal cancer risk, compared with that of populations carrying less than two low-risk genotypes (OR=0.74, 95%CI=0.58-0.95, P=0.017), especially in population of ≤68 years of age, male and BMI>25 kg/m^2, and non-smoking. Conclusions SNPs of mTORC1-related genes individually or jointly contribute to colorectal cancer susceptibility in Chinese. Further studies of larger cohorts are needed to validate the findings.

Objective: To compare different specimen types of lung adenocarcinoma in the detection of epidermal growth factor receptor (EGFR) gene and to correlate EGFR mutations with patient clinical features. Methods: One hundred lung adenocarcinoma cases were collected from June to December in 2015, at the First Affiliated Hospital of Xinjiang Medical University.Of the 100 lung adenocarcinoma samples, 43 were male and 57 were female. The age was from 40 to 88 years old, and the average age was 66 years. One hundred lung adenocarcinoma cases were divided equally into two groups. Mutation analysis of EGFR gene by real-time PCR was performed using biopsied tissue and paired blood samples in one group (n=50) and using pleural effusion and paired blood samples in the other group (n=50). Results: The mutation rate of EGFR gene in biopsy samples was 54% (27/50) , higher than that of blood samples (46%, 23/50), but without statistical differences (χ²=0.640, P=0.424). In contrast, mutation rate of EGFR gene in pleural effusion samples (42%, 21/50) was higher than that of blood samples (34%, 17/50), but without statistical differences(χ²=0.679, P=0.409). Two patients had EGFR mutation detected in paired blood samples but not in the corresponding biopsy samples, and four patients had EGFR mutation detected in pleural effusion samples but not in their paired blood samples. The mean progression-free survival of patients with detectable EGFR mutation were 9.5 months (tissue samples), 8.6 months (pleural effusion) and 8.5 months (blood). However, there was no statistical difference. Conclusions Blood samples may be used to assess EGFR mutations for patients with lung adenocarcinoma. However, further studies are needed to improve the sensitivity and accuracy in the detection of EGFR mutations using blood samples.