BACKGROUND:Now researches on psychiatric disease and molecular heredity are becoming more and more gradually because of the development of molecular genetics,but conclusions are controversial,and for the time being there are no reports about whether there are regional differences and ethnical differences in the distribution of genotype frequency of 5-hydroxytryptamine 2A receptor gene T102C.OBJECTIVE:Researches on the geographic distribution of genotype frequency of 5-hydroxytryptamine 2A receptor gene T102C of schizophrenics people.DESIGN:Sample survey and observation with schizophrenics selected as subjects.SETTING: Mental Department, Changzhou Peace Hospital.PARTICIPANTS: The experiment was completed in The No.102 Hospital of PLA from January 1999 to August 2003.Totally 177 people of Han nationality (Age: 18-45; Duration of illness: 1 month-20 years) from different provinces and autonomous regions of China in compliance with diagnostic standards of Psychiatric Disease Classification and Diagnosis Standards of China (The 3rd version) were selected as the subjects.METHODS:The blood samples from 117 schizophrenics were given test of polymerase chain reaction(PCR),and the distribution differences of genotype frequency of 5-hydroxytryptamine receptor gene of normal control population from different provinces and autonomous regions were compared. DNA were abstracted by means of phenol chloroform, amplification and cataphoresis test of polymerase chain reaction of target DNA,primer sequence of gene segment amplification of 5-hydroxytryptamine (5-HT) 2A receptor gene T102C: 5'-TCT GCT ACA AGT TCT GGC TT-3', 5 '-CTG CAG CTT TTT CTC TAG GG-3'; Reaction system of 50 μL, DNA 0.5 μg,Primer 50 pmol,TagDNA enzyme 2U were added with dNTP to the final concentration of 200 μmol/L.MAINOUTCOMEMEASURES: DNA cataphores is test of schiophrenicanddistributionofgenotypefrequencyof5-hydroxytryptamine 2A receptor gene.RESULTS: The distribution of genotype frequency of 5-hydroxytryptamine(5-HT) 2A receptor gene: A1A1, 0.07-0.03; A1A2, 0.50-0.72; A2A2,0.17-0.29. Correlation analysis of genotype frequency in different regions:A1A1, x2=4.44, P=0.617 1, P ＞ 0.05;A1A2, x2=1.14, P=0.942 2, P ＞ 0.05;A2A2, x2=0.93, P=0.985 7, P ＞ 0.05.CONCLUSION: The geographic distributions of genotype frequency of 5-hydroxytryptamine 2A receptor gene T102C of schizophrenics of the Chinese Han nationality people were comparatively even.

Objective To investigate the correlation between exposure of uric acid accumulation and the risks of acute pancreatitis(AP)in the population in Kailuan Group.Methods A prospective study was performed based on thesubjects receiving annual physical examination during 2006 to 2010 in Kailuan Group.All of them had no AP history but had complete data on UA.The starting point of follow-up was when the subjects completed the health examination in 2010,and the end point was new AP events,deaths or the end of follow-up(2021-12-31).Exposure of uric acid accumulation(cumUA)was calculated according to the average values of uric acid measured in each two consecutive physical examinations and the intervalbetween these two consecutive physical examinations.The cumulative incidences of AP indifferent subgroups(determined by the quartile of cumUA)were described using Kaplan-Meier product limit-method and compared by log-rank test.Multivariate Cox proportional hazards regression model was used to analyze the impacts of different cumUA subgroups on new occurrence of AP events.Results A total of 55,799 subjects were included in this study.The subjects were divided into four groups according to the quartile of cumUA.Sex ratio,average age,BMI,systolic blood pressure(SBP),diastolic blood pressure(DBP),FPG,TC,TG,LDL-C,HDL-C,smoking,alcohol consumption,education≥9 years,physical exercise,history of hypertension,and history of cholelithiasis differed significantly among the groups(P<0.05),there was no difference in diabetes history among the 4 groups(P=0.30).153 patients developed AP during an average follow-up of(10.52±1.75)years,the incidence rates were 1.65,2.76,2.13 and 3.96 per 10 000 person-year in the Q1,Q2,Q3and Q4,respectively(P<0.01).After adjusting sex,age,TC,TG,eGFR,smoking,alcohol consumption,education,physical activity,and history of hypertension,diabetes,or cholelithiasis,Multivariate analysis showed a significantly increased risk in Q4(HR=1.77,95%CI:1.07～2.92)as comparing with Q1.After excluding deaths during the follow-up period,Multivariate Cox regression analysis was performed again in Q4 HR=1.75(95%CI:1.04～2.95).Conclusions With the increase of cumUA exposure,both morbidity and risk of AP occur-rence have the tendency of rising.

Objective To explore the irradiation-increased krebs yon den lungen-6 (KL-6) in predicting radiation pneumonitis (RP) after lung cancer radiotherapy.Methods A total of 87 hospitalized patients with Ⅰ-Ⅲ stages of lung cancer from June 2015 to December 2015 were followed up,and their clinicopathological data and serum KL-6,transforming growth factor-beta 1 (TGF-β1)and lactate dehydrogenase (LDH)before and 3 months after radiotherapy were analyzed to determine their role in predicting RP induction in lung cancer.Results Among the 87 lung cancer patients based on clinical symptoms and chest CT,13 patients were diagnosed with ≥2 grape RP.Before radiotherapy,the average levels of serum KL-6 were (247 ± 105.44) U/ml in 13 patients with ≥ 2 grape RP and (209 ± 71.09) U/ml in 74 cases 0/1 grape RP,respectively.Within 3 months after radiotherapy,the highest level of KL-6 approached to (456 ± 202.84) and (222 ± 80.42) U/ml with increase ratios of 2.01 ± 1.04 and 1.13 ± 0.60 in the ≥2 grape RP and 0/1 grape RP,respectively.The difference of KL-6 levels between these two groups was significant (t =2.901,P ＜ 0.005).While the levels of TGF-β1 and LDH did not change.ROC analysis showed that the sensitivity of the ratio of serum KL-6 increased after radiotherapy was 0.923％ and the specificity was 0.851％ at 1.435 as the critical value.Furthermore,the multi-variate logistic regression analysis showed that the ratio of KL-6 increased as an independent risk factor of ≥ 2 grade RP in lung cancer (OR =12.886,95％ CI =3.372-49.247,P =0.002).Conclusions The increased ratio (≥ 1.435) of KL-6 is closely correlated with the ≥2 grape RP in lung cancer,which could be used as a predictor of ≥2 grape RP in lung cancer.

Objective To explore the value of serum neuron?specific enolase ( NSE ) before treatment in predicting brain metastases and prognosis of advanced non?small cell lung cancer ( NSCLC ) . Methods A total of 128 hospitalized patients with advanced NSCLC from Jan 2012 to Mar 2012 were followed up, and their clinicopathological data, serum NSE, carcinoembryonic antigen, cytokeratin 21?1 ( cyfra21?1 ) levels, albumin ( ALB ) , white blood cell ( WBC ) before treatment were analyzed retrospectively to determine the factors affecting brain metastasis and prognosis of advanced NSCLC. Results Among the 128 NSCLC patients, 90 cases were of adenocarcinoma, 30 cases were of squamous cell carcinoma, and 8 cases were of large cell carcinoma. The median levels of pre?treatment NSE, CEA and cyfra21?1 were 13.6 ng/ml, 7.8 ng/ml and 6.1 ng/ml, respectively. The average levels of ALB and WBC were(35.41±5.60)g/L and (8.16±2.53)×109/ml, respectively. Multi?variate logistic regression analysis showed that serum NSE before treatment was associated with brain metastasis of advanced NSCLC ( P=0.030). Pre?treatment NSE levels were (34.18±28.48) ng/ml in 28 patients with brain metastasis and (13.87±4.49) ng/ml in 98 patients without brain metastasis (P<0.05). The median survival time were 3.5 months in patients with normal levels of NSE, and 10.7 months in patients with elevated levels of NSE pre?treatment(P<0.05). Conclusions A higher pre?treatment level of NSE is closely correlated with brain metastasis of advanced NSCLC, and can be used as a predictor of brain metastases in advanced NSCLC. High pre?treatment levels of NSE indicate a poor prognosis in advanced NSCLC patients.

Background and objectiveIt has been proven that tumor necrosis factor receptor-associated factor 6 (TARF6) was a commonly ampliifed oncogene in lung cancer. However, the precise role of TARF6 protein in lung cancer has not been extensively investigated. hTis study analyzed the effects of TARF6 on the proliferation, apoptosis, cell cycle, migration, and invasion capability of lung cancer cell lines, as well as the potential molecular mechanisms involved.MethodsTo address the expression of TARF6 in lung cancer cells, four lung cancer cell lines (A549, H1650, SPC-A-1 and Calu-3) were assayed to determine the expression of TARF6 protein by Western blot and TARF6 mRNA via qRT-PCR. Moreover, siRNA targeting TARF6 was introduced into SPC-A-1 and Calu-3 cells. Nuclear factor-?B (NF-?B) DNA-binding activity, apoptosis rates, cell proliferation, cell cycle, migration, and invasion were determined by electrophoretic mobility shitf assay, lfow cytometry, MTS assay, lfow cytometry, scratch test, and transwell chamber assay, respectively. Western blot analysis was also performed to evalu-ate the expression of the following proteins through K63-ubiquitination: P65, CD24 and CXCR4. Whole-genome sequencing analysis was conducted using a second-generation sequencer in SPC-A-1 cells.Results TARF6 was highly up-expressed in SPC-A-1 and Calu-3 cell lines than the other two cells, which also showed K63-ubiquitinization in TARF6. However, consti-tutive activation of NF-?B was observed only in SPC-A-1 lung cancer cells. Downregulation of TARF6 suppressed the NF-κB activation, cell migration, and invasion but promoted the cell apoptosis of SPC-A-1 cells. Markedly decreased expression of CD24 and CXCR4 was observed in SPC-A-1 cells transfected by TARF6 siRNA. Nevertheless, TARF6 downregulation did not affect the proliferation and cell cycle of SPC-A-1 cells. Additionally, TARF6 regulation did not affect the proliferation, apoptosis, cell cycle, migration, and invasion of Calu-3 cells. No mutations and no changes in gene copy numbers of TARF6 were found by whole-exome sequencing of SPC-A-1 cells.ConclusionTARF6 may be involved in cell migration, invasion, and apoptosis of SPC-A-1 cells, possibly through regulating the NF-?B-CD24/CXCR4 pathway.

Objective To explore the value of serum neuron?specific enolase ( NSE ) before treatment in predicting brain metastases and prognosis of advanced non?small cell lung cancer ( NSCLC ) . Methods A total of 128 hospitalized patients with advanced NSCLC from Jan 2012 to Mar 2012 were followed up, and their clinicopathological data, serum NSE, carcinoembryonic antigen, cytokeratin 21?1 ( cyfra21?1 ) levels, albumin ( ALB ) , white blood cell ( WBC ) before treatment were analyzed retrospectively to determine the factors affecting brain metastasis and prognosis of advanced NSCLC. Results Among the 128 NSCLC patients, 90 cases were of adenocarcinoma, 30 cases were of squamous cell carcinoma, and 8 cases were of large cell carcinoma. The median levels of pre?treatment NSE, CEA and cyfra21?1 were 13.6 ng/ml, 7.8 ng/ml and 6.1 ng/ml, respectively. The average levels of ALB and WBC were(35.41±5.60)g/L and (8.16±2.53)×109/ml, respectively. Multi?variate logistic regression analysis showed that serum NSE before treatment was associated with brain metastasis of advanced NSCLC ( P=0.030). Pre?treatment NSE levels were (34.18±28.48) ng/ml in 28 patients with brain metastasis and (13.87±4.49) ng/ml in 98 patients without brain metastasis (P<0.05). The median survival time were 3.5 months in patients with normal levels of NSE, and 10.7 months in patients with elevated levels of NSE pre?treatment(P<0.05). Conclusions A higher pre?treatment level of NSE is closely correlated with brain metastasis of advanced NSCLC, and can be used as a predictor of brain metastases in advanced NSCLC. High pre?treatment levels of NSE indicate a poor prognosis in advanced NSCLC patients.

ObjectiveTo investigate the association between cumulative triglyceride （cumTG） exposure and the risk of acute pancreatitis （AP）. MethodsA prospective study was conducted for a cohort of 56 883 workers from Kailuan Group who participated in annual physical examination for three consecutive times in 2006-2010 （2006， 2008， and 2010） and had complete TG data without the medical history of AP. According to the quartiles of cumTG calculated， the subjects were divided into four groups （Q1， Q2， Q3， and Q4 groups）， and general information was compared between the two groups. A one-way analysis of variance was used for comparison of normally distributed continuous data between multiple groups， and the Kruskal-Wallis H test was used for comparison of continuous data with skewed distribution between multiple groups； the chi-square test was used for comparison of categorical data between groups. The Kaplan-Meier method was used to plot the survival curve and calculate the cumulative incidence rate of AP， and the Log-rank test was used for comparison between groups； the Cox regression model was used to analyze the effect of different cumTG levels on new-onset AP events. ResultsAfter follow-up for 10.51±1.76 years， there were 158 AP events in total， with a total incidence density of 2.64 per 10 000 person-years， and the number of cases and incidence density in the Q1， Q2， Q3， and Q4 groups were 29 cases （1.93 per 10 000 person-years）， 34 cases （2.27 per 10 000 person-years）， 30 cases （2.01 per 10 000 person-years）， and 65 cases （4.37 per 10 000 person-years）. The Log-rank test showed that there was a significant difference in cumulative incidence rate between groups （χ²=22.41， P<0.001）. The multivariate Cox regression analysis showed that compared with the Q1 group， the Q4 group had a significantly higher risk of AP （hazard ratio ［HR］=1.94， 95% confidence interval ［CI］： 1.20‍ ‍—‍ 3.13， P=0.01）. Compared with cumulative triglyceride exposure for 0 year， cumulative triglyceride exposure for 4 and 6 years significantly increased the risk of AP， with an HR value of 2.04 （95%CI： 1.26‍ ‍—‍ 3.30， P<0.01） and 3.20 （95%CI： 1.98‍ ‍—‍ 5.17， P<0.01）， respectively. After exclusion of the AP cases that occurred during the 2-year follow-up， the repeated multivariate Cox regression analysis showed that the Q4 group had an HR value of 1.96 （95%CI： 1.23‍ ‍—‍ 3.12， P<0.01） for the onset of AP， and after exclusion of the death cases during follow-up， the repeated multivariate Cox regression analysis showed that the Q4 group had an HR value of 1.85 （95%CI： 1.10‍ ‍—‍ 3.14， P<0.05） for the onset of AP. ConclusionThe incidence rate and risk of AP tend to increase with the increase in cumTG exposure.

OBJECTIVETo explore the value of serum neuron-specific enolase (NSE) before treatment in predicting brain metastases and prognosis of advanced non-small cell lung cancer (NSCLC).

METHODSA total of 128 hospitalized patients with advanced NSCLC from Jan 2012 to Mar 2012 were followed up, and their clinicopathological data, serum NSE, carcinoembryonic antigen, cytokeratin 21-1 (cyfra21-1) levels, albumin (ALB), white blood cell (WBC) before treatment were analyzed retrospectively to determine the factors affecting brain metastasis and prognosis of advanced NSCLC.

RESULTSAmong the 128 NSCLC patients, 90 cases were of adenocarcinoma, 30 cases were of squamous cell carcinoma, and 8 cases were of large cell carcinoma. The median levels of pre-treatment NSE, CEA and cyfra21-1 were 13.6 ng/ml, 7.8 ng/ml and 6.1 ng/ml, respectively. The average levels of ALB and WBC were (35.41 ± 5.60) g/L and (8.16 ± 2.53) × 10⁹/ml, respectively. Multi-variate logistic regression analysis showed that serum NSE before treatment was associated with brain metastasis of advanced NSCLC (P = 0.030). Pre-treatment NSE levels were (34.18 ± 28.48) ng/ml in 28 patients with brain metastasis and (13.87 ± 4.49) ng/ml in 98 patients without brain metastasis (P < 0.05). The median survival time were 3.5 months in patients with normal levels of NSE, and 10.7 months in patients with elevated levels of NSE pre-treatment (P < 0.05).

CONCLUSIONSA higher pre-treatment level of NSE is closely correlated with brain metastasis of advanced NSCLC, and can be used as a predictor of brain metastases in advanced NSCLC. High pre-treatment levels of NSE indicate a poor prognosis in advanced NSCLC patients.

Adenocarcinoma ; blood ; enzymology ; secondary ; Antigens, Neoplasm ; blood ; Brain Neoplasms ; secondary ; Carcinoembryonic Antigen ; blood ; Carcinoma, Large Cell ; blood ; enzymology ; secondary ; Carcinoma, Non-Small-Cell Lung ; blood ; enzymology ; secondary ; Carcinoma, Squamous Cell ; blood ; enzymology ; secondary ; Humans ; Keratin-19 ; blood ; Leukocyte Count ; Lung Neoplasms ; blood ; enzymology ; pathology ; Phosphopyruvate Hydratase ; blood ; Prognosis ; Retrospective Studies ; Serum Albumin ; analysis

After continuous development and improvement, lung transplantation has become the preferred means to treat a variety of benign end-stage lung diseases. However, the field of lung transplantation still faces many challenges, including shortage of donor resources, preservation and maintenance of donor lungs, and postoperative complications. Lung tissue samples removed after lung transplantation are excellent clinical resources for the study of benign end-stage lung disease and perioperative complications of lung transplantation. However, at present, the collection, storage and utilization of tissue samples after lung transplantation are limited to a single study, and unified technical specifications have not been formed. Based on the construction plan of the biobank for lung transplantation in the First Affiliated Hospital of Xi'an Jiaotong University, this study reviewed the practical experience in the collection, storage and utilization of lung transplant tissue samples in the aspects of ethical review, staffing, collection process, storage method, quality control and efficient utilization, in order to provide references for lung transplant related research.