In recent years， the incidence of pulmonary nodules has kept rising. To give full play to the advantages of traditional Chinese medicine （TCM） in the treatment of pulmonary nodules and identify the breakthrough points of integrating TCM with Western medicine， the China Association of Chinese Medicine organized medical experts in TCM and western medicine to carry out in-depth discussion regarding this disease. The discussion encompassed the modern medical advances， TCM theories of etiology and pathogenesis， the role and advantages of TCM in the whole course management of pulmonary nodules， contents and methods of research on pulmonary nodules， and science popularization work， aiming to provide a reference for clinical practice and scientific research. After discussion， the experts concluded that the occurrence of pulmonary nodules was rooted in the deficiency of the lung and spleen and triggered by phlegm dampness， blood stasis， and Qi stagnation. TCM can treat pulmonary nodules by controlling and reducing nodules， improving physical constitution， ameliorating multi-system nodular diseases， reducing anxiety and avoiding excessive diagnosis and treatment， and serving as an alternative for patients who are unwilling or unfit for surgical treatment. At present， the optimal diagnosis and treatment strategy for pulmonary nodules has not been formed， which needs to be further studied from multiple perspectives such as clinical epidemiology， biology， and evidence-based medicine. The primary task of current research is to find out the advantages， effective prescriptions， and target populations and determine the effective outcomes of TCM in the treatment of pulmonary nodules. At the same time， basic research should be carried out to explore the etiology and biological behaviors of pulmonary nodules. The expert consensus on the diagnosis and treatment of pulmonary nodules with integrated TCM and Western medicine needs to be continuously revised to guide clinicians to conduct standardized， scientific， and accurate effective diagnosis and treatment.

Objective:To investigate the status quo of psychological contracts and influencing factors among members of the "1+N" family doctor teams in Shenzhen and to explore the impact of psychological contracts on job burnout.Methods:This cross-sectional study was conducted from September 30 to October 31, 2022 among 361 members of 92 family doctor teams from 92 community health service centers which provided family doctor team service in Shenzhen city. A self-designed general information questionnaire, an employee psychological contract questionnaire (including organizational responsibility and personal responsibility dimensions), and a job burnout scale (including emotional exhaustion, depersonalization, and personal accomplishment dimensions) were used in the study. T-tests, one-way ANOVA, Pearson correlation analysis, and multiple linear regression analysis were used to analyze the influencing factors of psychological contracts and job burnout.Results:Among 361 respondents, there were 299 females (82.8%) and 62 males (17.2%), and a higher proportion of general practitioners (37.5%, 129/361) and nurses (41.8%, 151/361). The total score of psychological contracts among the 361 respondents was (141.6±19.5), with organizational responsibility scoring (70.6±11.2) and personal responsibility scoring (71.0±9.3). On the job burnout scale, emotional exhaustion scored (17.89±6.82), depersonalization scored (6.51±2.54), and personal accomplishment scored (30.95±5.70). General practitioners scored lower in organizational responsibility and personal responsibility compared to other members ( F=7.341,3.119, all P<0.05), and higher in emotional exhaustion and depersonalization ( F=7.637, 2.415, all P<0.05). Members with≤5 years of work experience scored lower in personal responsibility and personal accomplishment ( F=3.656, 4.205, all P<0.05). Correlation analysis showed that scores of organizational responsibility and personal responsibility were negatively correlated with levels of emotional exhaustion and depersonalization ( r=-0.618, -0.526, all P<0.01), ( r=-0.404, -0.393, all P<0.01), and positively correlated with personal accomplishment ( r=0.500, 0.558, all P<0.01). Multiple linear regression analysis indicated that organizational responsibility negatively affected emotional exhaustion and depersonalization ( β=-0.554, -0.274, all P<0.01), and positively affected personal accomplishment ( β=0.172, P<0.05). Personal responsibility positively affected personal accomplishment ( β=0.404, P<0.01). Conclusions:The study demonstrates that general practitioners in family doctor teams in Shenzhen city have lower psychological contract levels and are more prone to emotional exhaustion and depersonalization; members with≤5 years of work experience have lower personal responsibility and accomplishment. The results indicate that enhancing organizational responsibility can reduce job burnout of members in family doctor teams.

BACKGROUND:In recent years, based on high-throughput molecular imaging, integration of genomics, proteomics and computer aided design and the application of correlative “technical chains” have achieved great achievements in the research of breast cancer, lung cancer, gastric cancer, colon cancer, ovarian cancer and melanin tumor. However, there are few researches on oral squamous cel carcinoma. OBJECTIVE:To detect the gene expression profile of the oral squamous cel carcinoma tissue and normal paracarcinoma tissue using DNA chip-based gene expression profile. METHODS:Two samples of oral squamous cel carcinoma tissue and normal paracarcinoma tissue of patients who received treatment at Stomatological Hospital of Guangdong Province of China in 2013 were included in this study. The gene expression profiles of oral squamous cel carcinoma and normal paracarcinoma tissue were determined by the Roche NimbleGen gene expression microarrays. RESULTS AND CONCLUSION: According to screening criteria of differential genes, 7 872 out of 32 448 detected genes were differentialy expressed genes of oral squamous cel carcinoma, which accounts for 24% of the total number of the screening genes. 3 800 genes were up-regulated, and 4 072 were down-regulated. The results confirm that through detection with the help of gene expression profile clip, 7 872 differentialy expressed genes were obtained through DNA chip-based gene expression profiles according to the screening criteria. Thus it can be concluded that the occurrence and development of the tumors are not a result of single or several genes. Previous experiments based on a single or several genes have great limitations. These findings also suggest that the occurrence of tumor is a result of mutual regulatory effects of many genes forming a network, moreover, the interactions of the network is quite complicated.

Objective To investigate the expression of LKB1 and p53 in human gastric tissues and their correlation with clinical pathological factors.Methods The expression of LKB1 and p53 in 115 cases of gastric carcinoma and 20 cases of normal gastric tissues were detected by immunohistochemistry method,and the relation between the expression and the clinicopathological parameter of gastric carcinoma was analyzed.Results The positive rates of LKB1 in gastric carcinoma and normal tissues were 20.9 ％ (24/115) and 95.0 ％ (19/20),respectively (P ＜ 0.01).The positive rates of p53 in gastric carcinoma and normal tissues were 45.2 ％ (52/115) and 5.00 ％ (1/20),respectively (P ＜ 0.05).The analysis revealed that the high expression of LBK1 was associated with tumor lymph node metastasis,stage,Lauren classification and worse survival (P ＜ 0.05).The expression of p53 was associated with tumor lymph node metastasis,stage,distant metastasis and worse survival (P ＜ 0.05).Conclusions LKB1 protein expression may play an important role in the development and progression of gastric cancer.LKB1 may be used to assess the malignant biological behavior and prognosis of gastric cancer.

Objective To detect the expressions and clinical significance of Nanog and CD44 protein in lung cancer. Methods The expressions of Nanog and CD44 were detected by immunohistochemistry in 50 cases of lung cancer, 32 cases of benign lesion lung tissue and 18 cases of paraneoplastic normal lung tissue. Then their relationships with clinicopathological factors were analyzed. Results The expression of Nanog in lung cancer was significantly higher than those in benign lesion lung tissue and paraneoplastic normal lung tissue (P < 0.05). There was no significant difference of the expression of CD44 among the three groups (P > 0.05). The expressions of Nanog and CD44 in squamous cell carcinomas were higher than those in adenocarcinomas and small cell lung carcinomas (P < 0.05). The expressions of Nanog and CD44 were significantly correlated with lymph node metastasis (P < 0.05), but were not correlated with age, gender, tumour size, TNM stage and differentiation of lung cancer (P>0.05). The positive correlation was also noted between the expressions of Nanog and CD44 in lung cancer (r = 0.564, P < 0.05). Conclusion Nanog and CD44 proteins may participate in the genesis and progression of lung cancer. Nanog protein is a potential diagnostic marker and therapeutic target for lung cancer.

Background and purpose:Tumor suppressor gene P53 has long been studied in tumors, including breast cancer. More studies focused on the relationship between P53 and prognosis of breast cancer and found that P53 overexpression suggested a bad prognosis. However, the effect of P53 on early stage postmenopausal patients with ER-positive breast cancer has not been clariifed yet. This study was to investigate the role of P53 plays in aromatase inhibitor (AI) resistance among early stage postmenopausal patients with ER-positive breast cancer patients. Methods:A total number of 293 operable breast cancer patients who received surgical treatment during Jul. 2000 to Jul. 2006 in Fudan University Shanghai Cancer Center were enrolled into this study. All patients received AI treatment. The SPSS 12.0 software was used to estimate the survival rate. Univariate and multivariate analysis were also performed via above software. Results:The median follow-up time is 72 months (6-140 months). The 5 year disease free survival (DFS) of P53 positive and negative were 78%and 89%. The results showed that P53 overexpression (HR=1.729, 95%CI:1.038-2.880, P=0.035), pathological stage (HR=2.270, 95%CI:1.399-3.681, P=0.001);histological grade (HR=2.328, 95%CI:1.312-4.133, P=0.004); age (HR=1.988, 95%CI:1.511-2.617, P<0.005) were still the independent risk factors of recurrence and metastasis in breast cancer patients treated with AI. Conclusion:P53 overexpression correlated strongly with AI resistance in early stage postmenopausal patients with ER-positive breast cancer patients who were treated with AI and conifrmed the relevance of previously described prognostic factors. It is reasonable to take P53 expression into account when we evaluate the risk of breast cancer patients and decide the anti-cancer treatment strategy.

Objective To evaluate the safety, performability and long-term clinical efficacy of stenting angioplasty for treating symptomatic internal carotid artery (ICA) stenosis in the origin part in elderly patients. Methods Stenting angioplasty was performed on 29 patients with symptomatic ICA stenosis in the origin part. Results 29 stents were placed in 29 patients. Operations were performed 100%successfully. After an average 24 months of follow-up visits, restenoses were detected in 2cases reexamined by DSA 6 months after stenting, both presented with less than 50% stenoses. 1 case was found not regularly taking statins and antiplatelet drugs after stenting, severe restenosis occurred 6 months later, stent implantation performed again, no recurrence of transient ischemic attack (TIA) was noted during 2 years′follow-up visit. Cerebral ischemic strokes occurred in 2 cases , and both of them had balloon dilatation after stenting. 1 case was completely recovered after treatment and 1 was left with weakness in right extremities, unabling to walk. No cases of posterior circulation ischemia, death and myocardial infarction were detected. Conclusions Stenting angioplasty can be performed in treating symptomatic internal carotid artery stenosis in elderly patients. It showed a relatively good mid-long-term clinical effects and can be a secondary prevention option.

ObjectiveTo study the molecular genetic mechanism of para-bombay phenotype in two individuals.MethodsThe proband was a female.When the proband donated blood,because the forward blood group wasn't coincident with her reverse blood group,the blood and saliva specimen from proband and her family members were sent to Guangzhou Blood Center for further identification.Routine serological techniques were used to determine proband's and her family members' blood group and ABH antigen in saliva.The coding regions of FUT1 and FUT2 gene,exon 6 and exon 7 of ABO gene were amplified by polymerase chain reaction using proband's and her family members' genomic DNA.All amplified products were analyzed after being directly sequenced.The two-base deletion regions of FUT1 gene were certified by cloning and haplotype sequencing.Results Proband's and her little brother's blood group were identified as para-bombay while other family members' blood group were normal.Two-base deletion heterozygous mutations of FUT1 gene were found in proband and her brother,AG deletion at position 547-552 and TT deletion at position 880-882,which caused a reading frame shift and a premature stop eodon.Meanwhile,880-882del TT heterozygous mutation was found in proband's grandfather and her father and 547-552del AG heterozygous mutation was found in proband's mother and her little sister.ResultsOf cloning and haplotype sequencing certified that these two-base deletion mutations occurred at 547-548 and 881-882 position respectively.Three new mutations were found in FUT2 gene,390C ＞ T,418A ＞ T and 749G ＞ A,which could cause the change of amino acid at position 140Ile ＞ Phe and 250Arg ＞ Gln.Conclusions Two-base deletion heterozygous mutations in different positions in FUT1 gene were found in 2 individuals,which maybe the molecular genetic mechanism of para-bombay phenotype.Heterozygous deletion mutation in one-strand DNA wouldn't change the ABO blood group.Three new mutations were also found in FUT2 gene.( Chin J Lab Med,2012,35:815-819)

ObjectiveTo explore the effect of TLR4,PI3K and NF-κB on the migration of asthmatic airway smooth muscle cell(ASMCs) induced by airway epithelial cells.MethodsPrimary ASMCs were cultured by the method of cell digestion.Cell culture supernatant of RTE cells were collected by TNF-α stimulation of epithelial cells.Detected the IL-8 and RANTES levels in the supernatant.The effect of TLR4/PI3K-related signaling molecules on the migration of asthmatic ASMCs induced by epithelial cells were detected by Modified Boyden chemotaxis chamber with anti-TLR4 antibody,Wortmannin and PDTC drugs as a tool.ResultsThe levels of IL-8 and RANTES in the supernatant of TNF-αgroups were significantly increased,and that in the 20 ng/ml group was significantly higher than other groups ( P＜0.01 ).Compared with control group,the transmembrane migration of asthmatic ASMCs from other groups was significantly increased (P＜0.01 ).The transmembrane migration of asthmatic ASMCs from treated groups was significantly increased than asthma group (P＜0.01).The migration of asthmatic ASMCs from TNF-α+anti-TLR4 antibody group,TNF-α+Wortmannin group and TNF-α+Wortmannin+PDTC were significantly decreased than that of TNF-αgroup( P＜0.01 ).The migration of asthmatic ASMCs from TNF-α+Wortmannin+PDTC were significantly decreased than that of TNF-α+Wortmannin group (P＜0.05).ConclusionTLR4/PI3K-related signaling molecules involved in the transmembrane migration of asthmatic ASMCs induced by airway epithelial cells and may be one of the mechanisms of airway remodeling of asthma.

Objective To observe the effect of β-amyloid42 (Aβ42) on stimulating the inflammatory factors production by BV-2 microglia, including interleukin-1β (IL-1β), IL-10 and nitric oxide (NO), and to contrast the inhibitory action of anti-Aβ42 antibody in serum of Alzheimer's patients and the artificially synthesized anti-Aβ42 antibody. Methods The anti-Aβ42 antibodies were extracted from the serum of Alzheimer's patients. And the BV-2 microglia cells in murine were cultured as in vitro cell model. The cells were stimulated by Aβ42 and the two different anti-Aβ42antibodies to analyze the impact of stimulants on the cell activity. The Aβ42 of 5 μmol/L was added to the culture separately or in mixture with each of the two different anti-Aβ42 antibodies. Each antibody was mixed with Aβ42 of 5 μmol/L at final anti-Aβ42 antibody titre of 5 μg/ml, 1 μg/ml and 0.2 μg/ml,respectively. Then clear supernatant was collected from each tube respectively at 6 h, 12 h, and 24 h after culture, and the concentrations of IL-1β, IL-10 and NO were determined. Results The Aβ42,artificially synthesized anti-Aβ42 antibody and anti-Aβ42 antibody from Alzheimer's patients had no effects on the activities of BV-2 cells, the cell survival rates were (98. 6±5.8)%, (101.9±2.8)%and (98. 4±6.0)%, with no significant differences as compared with normal control group (F=0. 407, P＞0. 05). The inflammatory factors releasing from BV-2 cells stimulated by Aβ42 reached the peak level at 12 h, the concentrations of IL-1β, IL-10 and NO were (69.0±12.7) pg/ml, (24.1 ±4. 0) pg/ml and (128. 2±8. 7) μmol/L, the concentrations of IL-1β and NO were significantly higher at 12 h than at 6 h and 24 h (F= 15. 470 and 242. 107, P＜0.05), there was no significant difference in the concentration of IL-10 among 12 h, 6 h and 24 h (F=1. 852, P＞0.05). The two different antiAβ42 antibodies of different titre remarkably inhibited Aβ42 stimulated BV-2 cells to release inflammatory factors. At high titre of 5 μg/ml, the two different antibodies showed no significant difference in the inhibitory effects (P＞0.05), while at the titre of 0. 2 μg/ml, anti-Aβ42 antibody from Alzheimer's patients showed a significantly lower inhibitory effect than artificially synthesized antibodies, the concentrations of NO were (35.4 ± 2. 5) μoml/L and ( 19. 2 ± 3.3) μoml/L,respectively (P ＜ 0.05). Conclusions The Aβ42 can stimulate BV-2 microglia cells to release inflammatory factors. Anti-Aβ42 antibody from Alzheimer's patients has a lower inhibitory effect on Aβ42 in stimulating microglia to release inflammatory factors.