OBJECTIVETo investigate the role of allograft inflammatory factor-1 (AIF-1) in colorectal cancer (CRC) progression and explore the possible mechanism.

METHODSThe expression levels of AIF-1 in 70 CRC tissues and paired adjacent tissues were detected using immunohistochemistry and Western blotting, and the correlation of AIF-1 expression with the clinicopathological features of the patients was analyzed. In the CRC cell line SW480, the functional role of AIF-1 in regulating tumor progression was investigated by transfecting the cells with an AIF-1-overexpressing plasmid (AIF-1) and a negative control plasmid (NC). EdU proliferation assay and flow cytometry were used to assess the cell proliferation and cell cycle changes; Transwell migration assay and Annexin V-APC/7-AAD apoptosis assay kit were used to analyze the cell migration and apoptosis. The changes in the biological behaviors of the cells were observed after application of SB203580 to block the p38 MAPK pathway. The expression levels of CDK4, cyclin D1, P21, P27, MMP2, MMP9, Bax, Bcl2, Bcl-xl, p38 and p-p38 were detected using Western blotting.

RESULTSAIF-1 was down-regulated in CRC tissues compared with the adjacent normal tissues, and its expression level was positively correlated with lymph node metastasis (P=0.008), TNM stage (P=0.003) and tumor size (P=0.023). Overexpression of AIF-1 in SW480 cells significantly reduced EdU-positive cells and caused obvious cell cycle arrest in G1 phase (P<0.05). AIF-1 overexpression resulted in significantly lowered protein expressions of CDK4 and cyclin D1, enhanced expressions of P21 and P27, attenuated cell migration ability (P<0.001), and decreased protein levels of MMP2 and MMP9. AIF-1 overexpression also induced obvious apoptosis of SW480 cells (P<0.01), significantly increased the protein levels of Bax and p-p38, and decreased the protein levels of Bcl-2 and Bcl-xl; SB203580 significantly attenuated the apoptosis-inducing effect of AIF-1 overexpression.

CONCLUSIONAIF-1 plays the role of a tumor suppressor in CRC by inhibiting cell proliferation, suppressing cell migration and inducing cell apoptosis. AIF-1 overexpression promotes the apoptosis of CRC cells by activating the p38 MAPK pathway.

OBJECTIVETo investigate and analyze the clinicopathological features and choice of treatment for delayed inhaled bronchial foreign bodies.

METHODSA retrospective review is presented of patients with delayed inhaled bronchial foreign bodies treated by pulmonary resection between January 1980 and June 2010. There were 17 patients (12 male and 5 female). Mean age was 36 years (ranging 10 to 66 years). The mean interval of onset was 2 years (ranging 3 months to 8 years). Confirmed diagnosis before surgery in 8 cases and 9 cases were misdiagnosed as other diseases. Surgical procedures included right lower lobectomy in 4 cases, right middle lobectomy in 3 cases, right lower and middle lobectomy in 1 case, right lobe lobectomy and rid resection drainage in 1 case, right lobe lobectomy and pleurectomy in 1 case, video-assisted right lobe partial resection in 1 case, left pneumonectomy in 4 cases, left lower lobectomy in 1 cases and left upper lobectomy in 1 cases.

RESULTSOne case died of pulmonary infection and 2 cases complicated of BPF after operation. Foreign bodies were localized in the right bronchial tree in 11 cases, the left in 6 cases. The majority of the foreign bodies were vegetable origin.

CONCLUSIONSThe diagnosis rate of delayed inhaled bronchial foreign bodies should be improved in order avoiding of pulmonary resection. It is necessary to perform pulmonary resection timely if the pulmonary infection is evident for fear that the infection progress into severe infection.

Adolescent ; Adult ; Aged ; Bronchi ; Child ; Female ; Foreign Bodies ; surgery ; Humans ; Male ; Middle Aged ; Pneumonectomy ; Retrospective Studies ; Treatment Outcome ; Young Adult

BACKGROUNDIt has already been recognized that psychosocial stress evokes asthma exacerbation; however, the mechanism of how stress gets inside the body is not clear. This study aimed to observe the impact of psychosocial stress on airway inflammation and its mechanism in the ovalbumin-induced asthmatic mice combined with social disruption stress.

METHODSThirty-six male BALB/c mice were randomly divided into: control group, asthma group (ovalbumin-induced), asthma plus social disruption stress group (SDR), and SDR group. The open field video tracking system was used to assess animal behaviors. The invasive pulmonary resistance (RL) and dynamic lung compliance (cdyn) test system from Buxco was applied to detect pulmonary function. The enzyme-linked immunosorbent assay (ELISA) was utilized to determine OVA-IgE, T-helper type 2 (Th2) cytokines (IL-4, IL-5, IL-13) and corticosterone in mouse serum, the Th2 cytokines (IL-4, IL-5, IL-13, IL-6, TNF-α) in bronchoalveolar lavage fluid (BALF), and IL-6 and TNF-α levels in the supernatant of splenocytes cultured in vitro. Hematoxylin-eosin (H&E) staining was used to assess airway inflammation in lung histology. The cell count kit-8 assay (CCK-8) was applied to evaluate the inhibitory effect of corticosterone on splenocyte proliferation induced by lipopolysaccharide (LPS). Real time-PCR and Western blotting were utilized to determine glucocorticoid receptor (GR) mRNA and GR protein expression in lungs.

RESULTSThe open field test showed that combined allergen exposure and repeated stress significantly shortened the time the mice spent in the center of the open field (P < 0.01), increased ambulatory activity (P < 0.01) and the count of fecal boli (P < 0.01), but deceased vertical activity (P < 0.01). Results from pulmonary function demonstrated that airway hyperresponsiveness (AHR) was enhanced by psychosocial stress compared with allergy exposure alone. The ELISA results showed that cytokines in serum and BALF were significantly increased (P < 0.05). Moreover, the lung histology showed that infiltrated inflammatory cells were significantly increased in the asthma-SDR group compared with the asthma group (P < 0.05). Interestingly, serum corticosterone was remarkably raised by psychosocial stress (P < 0.05). In addition, the inhibitory effect of corticosterone on IL-6 and TNF-α in LPS-stimulated splenocyte cultures in vitro was diminished in the asthma-SDR group compared to the asthma group. The CCK-8 test revealed that the inhibition effect of corticosterone on splenocyte proliferation induced by LPS was significantly impaired in the SDR and asthma-SDR groups, while no significant effect was observed in the control and asthma groups. Furthermore, expression of GR mRNA and GR protein were significantly reduced in the lung tissues of the asthma-SDR group (P < 0.05).

CONCLUSIONSSocial disruption stress can promote anxiety behavior, activate the hypothalamic-pituitary-adrenal (HPA) axis, increase AHR and inflammation, and also impair glucocorticoid sensitivity and its function in a murine model of asthma. The down-regulation of GR expression induced by social disruption stress is in part associated with glucocorticoid insensitivity, which leads to asthma exacerbation.

Animals ; Anxiety ; etiology ; Asthma ; etiology ; Bronchial Hyperreactivity ; etiology ; Corticosterone ; blood ; Cytokines ; biosynthesis ; Disease Models, Animal ; Lung ; pathology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Receptors, Glucocorticoid ; analysis ; physiology ; Stress, Psychological ; complications

【Objective】 To evaluate the clinical value of 18F-FDG PET/CT features in differentiating lymphovascular infiltration in patients with solid stage I lung adenocarcinoma. 【Methods】 From January 2017 to September 2019, a total of 86 patients [43 males and 43 females; age(59.9 ± 10.3) years; age range: 28-81 years] with surgically and pathologically confirmed stage I lung adenocarcinomas were included. All patients received ¹⁸F-FDG PET/CT examination preoperatively and were divided into positive and negative groups according to the histopathological lymphovascular infiltration status. Patient gender, age, lesion location, HRCT features(size, sharp, lobulated sign, spiculated sign, bubble lucency, air bronchogram sign, pleural traction and para-tumor emphysema) and SUVmax(maximum of standard uptake value) were recorded and compared using univariate analysis between lymphovascular infiltration positive and negative groups, respectively. Logistic regression analysis was used to establish a predictive model between PET/CT parameters and lymphovascular infiltration status. Receiver operating characteristic(ROC) analysis was performed to assess the diagnostic performance and determined the cutoff values. 【Results】 There were 12 cases [5 males and 7 females; age: (59.0±8.3) years] in the lymphovascular infiltration positive group and 74 cases [38 males and 46 females; age: (60.1±10.6) years] in the negative group. Significant statistical differences were shown in lesion size、sharp and SUVmax between the two groups (Z = -2.505, P = 0.012; P = 0.048; t = -3.625, P = 0.003). SUVmax was an independent risk factor for positive in multivariation logistic regression analysis(OR value: 1.484; 95%CI: 1.195-1.843; P = 0.000). The optimum cut-off value for positive was greater than 7.75 mm in the ROC curve analysis and the area under curve(AUC), sensitivity, specificity and accuracy was 0.840, 75.0%, 79.7% and 79.1%, respectively. 【Conclusions】 The PET/CT characteristics may be useful in differentiating lymphovascular infiltration status in patients with solid stage I lung adenocaricinoma. SUVmax was an independent risk factor and greater than 7.75 were more likely to be lymphovascualr infiltration, which will be helpful for selection of treatment pattern.