Gastrointestinal syndrome encountered during a train voyage to high altitudes: A 14-day survey of 69 passengers in China.

BACKGROUND: The diagnosis and evaluation of the severity of acute mountain sickness (AMS) continue to be problematic due to a lack of consensus on the inclusion of symptoms in a scoring system. Recent investigations highlight the significance of gastrointestinal symptoms in identifying this condition. However, the specific gastrointestinal symptoms associated with AMS have not been thoroughly elucidated in previous studies, and the underlying risk factors remain inadequately comprehended. METHODS: This study aimed to investigate the characteristics, trends, and risk factors related to gastrointestinal symptoms encountered during train travel to high altitude. A total of 69 passengers, specifically all with medical backgrounds, were surveyed 6 times over a period of 14 days. RESULTS: The daily incidence of abdominal discomfort was higher than non-gastrointestinal symptoms within 14 days. Gastrointestinal symptoms demonstrated a greater prevalence, longer duration, and increased risk compared to non-gastrointestinal symptoms, such as headaches. The symptoms of abdominal distension and bowel sound hyperaction were found to be prevalent and persistent among patients diagnosed with AMS, exhibiting a high incidence rate. Gender, age, body mass index (BMI), smoking habits, and alcohol consumption were identified as risk factors associated with the occurrence and duration of gastrointestinal symptoms. CONCLUSION: This study suggests that gastrointestinal symptoms are more common and persistent when traveling to the plateau by train. These symptoms should be taken into consideration in the further diagnosis and prevention of AMS. Therefore, this study provides a significant theoretical foundation for the prevention and treatment of AMS.

Establishment of Routine Clinical Indicators-Based Nomograms for Predicting the Mortality in Patients With COVID-19.

This study aimed to establish and validate the nomograms to predict the mortality risk of patients with coronavirus disease 2019 (COVID-19) using routine clinical indicators. This retrospective study included a development cohort enrolled 2,119 hospitalized patients with COVID-19 and a validation cohort included 1,504 patients with COVID-19. The demographics, clinical manifestations, vital signs, and laboratory tests of the patients at admission and outcome of in-hospital death were recorded. The independent factors associated with death were identified by a forward stepwise multivariate logistic regression analysis and used to construct the two prognostic nomograms. The nomogram 1 was a full model to include nine factors identified in the multivariate logistic regression and nomogram 2 was built by selecting four factors from nine to perform as a reduced model. The nomogram 1 and nomogram 2 showed better performance in discrimination and calibration than the Multilobular infiltration, hypo-Lymphocytosis, Bacterial coinfection, Smoking history, hyper-Tension and Age (MuLBSTA) score in training. In validation, nomogram 1 performed better than nomogram 2 for calibration. We recommend the application of nomogram 1 in general hospitals which provide robust prognostic performance though more cumbersome; nomogram 2 in the out-patient, emergency department, and mobile cabin hospitals, which depend on less laboratory examinations to make the assessment more convenient. Both the nomograms can help the clinicians to identify the patients at risk of death with routine clinical indicators at admission, which may reduce the overall mortality of COVID-19.

Echocardiographic Right Ventricular Outflow Track Notch Formation and the Incidence of Acute Mountain Sickness.

Yuan, Fangzhengyuan, Zhexue Qin, Chuan Liu, Shiyong Yu, Jie Yang, Jun Jin, Shizhu Bian, Xubin Gao, Jihang Zhang, Chen Zhang, Mingdong Hu, Jingbin Ke, Yuanqi Yang, Jingdu Tian, Chunyan He, Wenzhu Gu, Chun Li, Rongsheng Rao, and Lan Huang. Echocardiographic right ventricular outflow track notch formation and the incidence of acute mountain sickness. High Alt Med Biol. 22:263-273, 2021. Background: High-altitude exposure causes acute mountain sickness (AMS) and increases pulmonary arterial pressure (PAP). The notching of echocardiographic right ventricular outflow tract flow velocity envelope (right ventricular outflow tract [RVOT] notching), is related to increased PAP. We speculate that acute high-altitude exposure may trigger RVOT notching, which may be associated with AMS. Methods: All 130 subjects, ascended to 4,100 m from low altitude by bus within 7 days, underwent physiological and echocardiographic testing. The subjects with a total score of 3 or above and in the presence of a headache were diagnosed with AMS according to Lake Louise criteria. Results: After high-altitude exposure, the incidence of RVOT notching and AMS was 20% and 28.5%, respectively. The subjects with AMS had a higher incidence (37.8%) of RVOT notching than those without AMS (12.9%). Multivariate logistic regression analysis showed that RVOT notching was associated with systolic pulmonary artery pressure (SPAP) (odds ratio [OR], 1.11; 95% confidence interval [CI], 1.05-1.17; p < 0.001) and the occurrence of AMS (OR, 5.48; 95% CI, 1.96-15.35; p = 0.001). Although linear regression analysis showed a weak correlation between SPAP and Lake Louise AMS score in the overall population (r = 0.20, p = 0.020), this correlation was more pronounced in the subpopulation with RVOT notching (r = 0.44, p = 0.023) and SPAP was not related to Lake Louise AMS score in the subpopulation without RVOT notching (r = 0.03, p = 0.698). Among AMS symptoms, the incidence of headache and fatigue were higher in subjects with RVOT notching than those in subjects without RVOT notching. Conclusions: We first observe that high-altitude exposure triggers RVOT notching formation, which is associated with AMS occurrence. Clinical Trials.gov ID: ChiCTR-RCS-12002232.

Pulmonary function tests at low altitude predict pulmonary pressure response to short-term high altitude exposure.

BACKGROUND: Travelling to high altitude (HA) presents a risk of the high levels of pulmonary artery pressure (PAP) at altitude, which is associated with impaired exercise capacity and fatal HA pulmonary oedema. However, prediction of high levels of PAP at altitude is still unclear. METHODS: Echocardiography and pulmonary function tests were performed on 121 healthy men at low altitude (LA) and 4100 m (5 ± 2 h after a 7 day ascent). RESULTS: HA exposure increased the levels of FEV1/FVC ratio, FEF25%, 50%, 75%, MMEF, mPAP, total pulmonary vascular resistance (PVR) and systolic pulmonary arterial pressure (SPAP). More smokers and lower forced expiratory flow at 25% of forced vital capacity (FEF25%) at LA were observed in subjects with mPAP≥30 mmHg than those with mPAP<30 mmHg at HA. Multivariate logistic regression identified that FEF25% at LA [odds ratio (OR) 0.50, 95%CI 0.33-0.76, p = 0.001] and smoking (OR 3.09, 95%CI 1.31-7.27, p = 0.010) were the independent predictors for identifying subjects with mPAP≥30 mmHg at HA. Moreover, FEF25% at LA was linearly correlated with mPAP at HA (r = -0.31, p < 0.001), which mainly existed in smokers. Compared to subjects with FEF25% ≥7.55 L/sec at LA, those with FEF25% <7.55 L/sec at LA showed higher levels of mPAP, and total PVR, and a multivariable OR of 11.16 (95%CI, 3.48-35.81) for developing mPAP ≥ 30 mmHg at HA. However, there was no significant difference in the incidences of AMS and its related clinical symptoms in subjects with different levels of FEF25%. CONCLUSIONS: Thus, these findings suggest that subjects with low FEF25% values at LA are susceptible to high levels of PAP at altitude but not the incidence of AMS following short-term HA exposure, especially in smokers.

Efficacy of Shenqi Pollen Capsules for High-Altitude Deacclimatization Syndrome via Suppression of the Reoxygenation Injury and Inflammatory Response.

High-altitude deacclimatization syndrome (HADAS) is involved in hypoxia-reoxygenation injury and inflammatory response, induced a series of symptoms, and has emerged as a severe public health issue. Here, we investigated the mechanism as well as potential means to prevent HADAS using Shenqi pollen capsules (SPCs) in subjects with HADAS in a multicenter, double-blinded, randomized, placebo-controlled study. All subjects were at the same high altitude (3650 m) for 4-8 months before returning to lower altitudes. Subjects (n = 288) in 20 clusters were diagnosed with mild or moderate HADAS on the third day of the study. We randomly allocated 20 clusters of subjects (1 : 1) to receive SPCs or a placebo for 7 weeks, and they were then followed up to the 14th week. The primary endpoints were subjects' HADAS scores recorded during the 14 weeks of follow-up. Compared with the placebo, SPC treatment significantly decreased the subjects' HADAS scores and reduced the incidence of symptom persistence. SPC therapy also reduced the serum levels of CK, CK-MB, LDH, IL-17A, TNF-α, and miR-155 and elevated IL-10 and miR-21 levels. We thus demonstrate that SPCs effectively ameliorated HADAS symptoms in these subjects via suppression of the hypoxia-reoxygenation injury and inflammatory response.

The Role of SIRT1 in Autophagy in Lipopolysaccharide-Induced Mouse Type II Alveolar Epithelial Cells.

Silent mating type information regulation 2 homolog-1 (SIRT1) is involved in a wide range of cellular processes because of its role as a deacetylated histone and its association with a variety of transcription factors. SIRT1 has essential roles in autophagy, including in the formation of autophagic vacuoles and the assembly of autophagy-related gene (ATG) protein complexes. The present study focused on the role of SIRT1 in autophagy in lipopolysaccharide (LPS)-induced mouse type II alveolar epithelial cells (AECII). We designed experiments using SIRT1-overexpressing mice and wild-type mice, and AECII were isolated from these two types of mouse for in vitro LPS injury trials. Our results suggest that levels of the autophagy proteins, Beclin1 and LC3B, as well as those of the inflammatory factors, IL-6 and TNF-α, were increased in LPS-induced mouse AECII, and that SIRT1 protected against damage in mice with acute respiratory distress syndrome and in mouse AECII in vitro following LPS treatment. Subsequently, we screened multiple inflammatory, apoptotic, and unclassified genes (including Atg7), which interacted with SIRT1 in LPS-injured mouse AECII, as assessed by mRNA microarray analysis. These results demonstrate that LPS can reduce the levels of SIRT1 and ATG7 in vivo and in vitro and indicate that SIRT1 is involved in autophagy through regulation of ATG7 in AECII in response to LPS.

Activation of PPARγ inhibits pro-inflammatory cytokines production by upregulation of miR-124 in vitro and in vivo.

Peroxisome proliferator-activated receptor gamma (PPARγ) and miR-124 have been reported to play important roles in regulation of inflammation. However, the underlying anti-inflammatory mechanisms remain not well understood. In the present study, we demonstrated that the expression level of PPARγ is positively correlated with that of miR-124 in patients with sepsis. Activation of PPARγ upregulates miR-124 and in turn inhibits miR-124 target gene. PPARγ bound directly to PPRE in the miR-124 promoter region, and enhanced the promoter transcriptional activity. PPARγ-induced miR-124 is involved in the suppression of pro-inflammatory cytokine in vitro and in vivo. These results suggest that PPARγ-induced miR-124 inhibits the production of pro-inflammatory cytokines is a novel PPARγ anti-inflammatory mechanism and also indicate that miR-124 may be a potential therapeutic target for the treatment of inflammatory diseases.

Association between Serum Interleukin-17A Level and High-Altitude Deacclimatization Syndrome.

High-altitude deacclimatization syndrome (HADAS) is emerging as a severe public health issue that threatens the quality of life of individuals who return to lower altitude from high altitude. In this study, we measured serum levels of SOD, MDA, IL-17A, IL-10, TNF-α, and HADAS score in HADAS subjects at baseline and 50th and 100th days and to evaluate the relationship between interleukins, including IL-17A, and HADAS. Our data showed that and the serum IL-17A levels and HADAS score decreased over time in the HADAS group, and serum IL-17A levels were significantly higher in the HADAS group at baseline and 50th day compared with controls (p < 0.05). Furthermore, baseline serum levels of MDA and TNF-α were significantly higher, while SOD and IL-10 levels were lower in HADAS subjects compared with controls (p < 0.05). It is interesting that serum levels of IL-17A were clearly interrelated with HADAS incidence and severity (p < 0.05). ROC curve analysis showed that combined serum IL-17A and IL-10 levels were a better predictor of HADAS incidence than serum levels of IL-17A or IL-10 alone. These data suggest that serum levels of IL-17A are a novel predictive index of HADAS.

Uncoupling Protein 2 Increases Susceptibility to Lipopolysaccharide-Induced Acute Lung Injury in Mice.

Uncoupling protein 2 (UCP2) is upregulated in patients with systemic inflammation and infection, but its functional role is unclear. We up- or downregulated UCP2 expression using UCP2 recombinant adenovirus or the UCP2 inhibitor, genipin, in lungs of mice, and investigated the mechanisms of UCP2 in ALI. UCP2 overexpression in mouse lungs increased LPS-induced pathological changes, lung permeability, lung inflammation, and lowered survival rates. Furthermore, ATP levels and mitochondrial membrane potential were decreased, while reactive oxygen species production was increased. Additionally, mitogen-activated protein kinases (MAPKs) activity was elevated, which increased the sensitivity to LPS-induced apoptosis and inflammation. LPS-induced apoptosis and release of inflammatory factors were alleviated by pretreatment of the Jun N-terminal kinase (JNK) inhibitor SP600125 or the p38 MAPK inhibitor SB203580, but not by the extracellular signal-regulated kinase (ERK) inhibitor PD98059 in UCP2-overexpressing mice. On the other hand, LPS-induced alveolar epithelial cell death and inflammation were attenuated by genipin. In conclusion, UCP2 increased susceptibility to LPS-induced cell death and pulmonary inflammation, most likely via ATP depletion and activation of MAPK signaling following ALI in mice.

Extraction of polysaccharides from Fomes officinalis Ames and their antitumor activity.

The aim of this study was to optimize the extraction parameters of Fomes officinalis Ames polysaccharides (FOAPs) and evaluate their antitumor activity. FOAPs were extracted using the hot water extraction, acid extraction and alkali extraction methods, respectively. Alcohol precipitation and acetone washes were conducted to separate and purify the FOAPs. The FOAP content was determined using the phenol-sulfuric acid method. The effects of raw material particle size, extraction time and material-liquid ratio on the yield of FOAPs were investigated, and the effects of FOAPs on the immune function of S180 tumor-bearing mice and their antitumor activity were evaluated. The yield of FOAPs obtained with the hot water extraction method was higher compared with the yields of the other methods. The optimum extraction conditions were as follows: a raw material particle size of 24 mesh; an extraction time of 2.5 h; and a material-liquid ratio of 1 g:12 ml. Under these conditions, the yield of FOAPs was 1.13%. FOAPs significantly inhibited tumor growth and enhanced the immune function in S180 tumor-bearing mice. FOAPs extracted using the hot water extraction method have antitumor activity.

The cyclin D1 (CCND1) G870A polymorphism and lung cancer susceptibility: a meta-analysis.

Several studies have investigated the association between Cyclin D1 (CCND1) G870A genetic polymorphism and lung cancer susceptibility, but the results were inconclusive. The aim of this meta-analysis was to summarize available evidence for such a relationship. The reviewers made use of MEDLINE, EMBASE, and BIOSIS databases. The relevant data were independently extracted by two reviewers. The odds ratio (OR) with 95% confidence interval (CI) was selected as the principal outcome measure. The heterogeneity test, the publication bias test, and the sensitivity analysis were performed. Overall, a total of 10 case-control studies were included. Our meta-analysis indicated that CCND1 G870A genetic polymorphism was a risk factor for lung cancer under homozygote model (OR = 1.18; 95% CI = 1.02, 1.37), recessive model (OR = 1.21; 95% CI = 1.03, 1.41), and allele model (OR = 1.11; 95% CI = 1.02, 1.21). In the subgroup analysis by source of ethnicity, a statistical increase of lung cancer risk was found among Asian groups for allele model (OR = 1.11; 95% CI = 1.01-1.22). The present meta-analysis suggests that CCND1 G870A polymorphism may be a risk factor for lung cancer. Besides, allele A may contribute to increased lung cancer risk.

Hypoxia-inducible factor 1 promoter-induced JAB1 overexpression enhances chemotherapeutic sensitivity of lung cancer cell line A549 in an anoxic environment.

The presence of lung cancer cells in anoxic zones is a key cause od chemotherapeutic resistance. Thus, it is necessary to enhance the sensitivity of such lung cancer cells. However, loss of efficient gene therapeutic targeting and inefficient objective gene expression in the anoxic zone in lung cancer are dilemmas. In the present study, a eukaryotic expression plasmid pUC57-HRE-JAB1 driven by a hypoxia response elements promoter was constructed and introduced into lung cancer cell line A549. The cells were then exposed to a chemotherapeutic drug cis-diamminedichloroplatinum (C-DDP). qRT-PCR and western blotting were used to determine the mRNA and protein level and flow cytometry to examine the cell cycle and apoptosis of A549 transfected pUC57-HRE-JAB1. The results showed that JAB1 gene in the A549 was overexpressed after the transfection, cell proliferation being arrested in G1 phase and the apoptosis ratio significantly increased. Importantly, introduction of pUC57-HRE-JAB1 significantly increased the chemotherapeutic sensitivity of A549 in an anoxic environment. In conclusion, JAB1 overexpression might provide a novel strategy to overcome chemotherapeutic resistance in lung cancer.

Pretreatment with anti-flagellin serum delays acute lung injury in rats with sepsis.

OBJECTIVE: This study examined the reduction of sepsis-induced ALI by inhibition of flagellin-stimulated TLR5 signaling. METHODS: Rats were randomly divided into three groups: one group served as the sham-operated group (control group), and the other two groups received the induction of sepsis (sepsis and treatment groups). The treatment group was injected with anti-flagellin serum before induction of sepsis. At 2, 4, 6, 12, 24, and 48 h following induction of sepsis (six time-point subgroups, n = 10 per subgroup), arterial PaO(2), wet/dry (W/D) lung weight ratios, levels of serum and BALF flagellin and TNF-α, pulmonary pathological alterations, and TLR5 mRNA expression in the lungs were examined. RESULTS: Compared to sham-operated rats, septic rats had: increased levels of serum and BALF flagellin at 6, 12, 24, and 48 h; reduced arterial PaO(2); elevated W/D lung weight ratio; increased serum and BALF TNF-α levels; and up-regulated TLR5 mRNA expression at 12, 24, and 48 h (P < 0.01). Pretreatment with anti-flagellin serum, however, significantly inhibited sepsis-associated declines in arterial PaO(2), increased W/D lung weight ratios, elevated serum and BALF TNF-α levels, and up-regulated TLR5 mRNA expression at 24 and 48 h (P < 0.01). CONCLUSION: Neutralizing the actions of circulating flagellin with anti-flagellin serum delayed the development of ALI in rats with sepsis.

[The effects of Ad-Gax transfection on apoptosis and related gene expression in pulmonary arterial smooth muscle cells in hypoxic rat model].

OBJECTIVE: To explore the effects of growth arrest-specific homeobox (Gax) transfection on apoptosis and expressions of Bcl-2 and Bax proteins of rat pulmonary arterial smooth muscle cells (PASMCs) exposed to hypoxia. METHODS: PASMCs were transfected with Gax gene by a replication-deficient adenovirus expressing the hemagglutinin-tagged Gax cDNA (Ad-Gax). After exposure to normal oxygenation (21% O(2)) or hypoxia (2.5% O(2)) for 2 h, 6 h, 12 h, 24 h and 48 h, apoptosis was observed by transmission electronic microscope and TUNEL-positive staining. The expressions of Bcl-2 and Bax proteins in PASMCs were detected by immunocytochemistry. RESULTS: Before Ad-Gax transfection, none or few of TUNEL-positive PASMCs were detected. After Ad-Gax transfection, the PASMCs unexposed to hypoxia displayed none or few TUNEL-positive stain, while the PASMCs exposed to hypoxia displayed a marked increase in TUNEL-positive stain, especially in cells exposed to hypoxia for 24 h to 48 h. The ratio of apoptosis of PASMCs at normoxic, hypoxia 2 h, 6 h, 12 h, 24 h and 48 h were (9.11 +/- 1.21)%, (34.13 +/- 1.02)%, (39.12 +/- 0.43)%, (50.09 +/- 0.13)%, (60.04 +/- 1.12)% and (55.47 +/- 0.03)% (P < 0.01), respectively. Before Ad-Gax transfection, the level of Bax protein showed no significant increase in PASMCs exposed to hypoxia, while that of Bcl-2 protein increased significantly, as compared to that in PASMCs under normoxic condition. The average optical density (AOD) of Bcl-2 was 2.31 +/- 0.12, 2.35 +/- 0.23, 2.49 +/- 0.27, 2.51 +/- 0.19, 2.54 +/- 0.25 and 2.53 +/- 0.20 at normoxic, hypoxia for 2 h, 6 h, 12 h, 24 h and 48 h before Ad-Gax transfection, respectively (P < 0.05, P < 0.01). After Ad-Gax transfection to PASMCs exposed to hypoxia, Bax protein increased; the AOD of Bax was 3.82 +/- 0.38, 3.12 +/- 0.42, 3.53 +/- 0.61, 4.52 +/- 0.23, 4.25 +/- 0.76 and 4.03 +/- 0.38 at normoxic, hypoxia for 2 h, 6 h, 12 h, 24 h and 48 h (P < 0.01), respectively. But Bcl-2 protein decreased significantly; the AOD of Bcl-2 was 9.11 +/- 1.21, 34.13 +/- 1.02, 39.12 +/- 0.43, 50.09 +/- 0.13, 60.04 +/- 1.12 and 55.47 +/- 0.03, respectively (P < 0.01). After Ad-Gax transfection, the Bcl-2/Bax ratio was negatively correlated with the rate of apoptotic PASMCs (r = -0.53, P < 0.01). CONCLUSION: Ad-Gax transfection induced PASMC apoptosis after exposure to hypoxia. A possible mechanism is that Gax can downregulate Bcl-2 expression and upregulate Bax expression, especially by decrease of the Bcl-2/Bax ratio.

[Effect of Ad-Gax transfection on apoptosis of human lung adenocarcinoma A549 cells and its mechanism].

BACKGROUND: Apoptosis is closely related to development of lung cancer. It is a strategy of lung cancer therapy to induce apoptosis. The aim of this study is to explore the effects of growth arrest-specific homeobox (Gax) transfection on apoptosis and expression of Bcl-2 and Bax proteins of human lung adenocarcinoma A549 cells. METHODS: A549 cells were transfected with Gax gene by a replication-deficient adenovirus expressing the hemagglutinin-tagged Gax cDNA (Ad-Gax). Apoptosis of A549 cells was observed by transmission electronic microscope and terminal-deoxynucleotidyl transferase mediated nick end labeling (TUNEL) positive staining. Apoptotic rate of A549 cells was evaluated by flow cytometry. Expressions of Bcl-2 and Bax proteins in A549 cells were detected by immunocytochemistry. RESULTS: Before Ad-Gax transfection, none or few of TUNEL-positive A549 cells were detected. After Ad-Gax transfection, a marked increase in TUNEL-positive staining occurred, especially at 24 h later. The ratio of apoptosis of A549 cellsin non-transfection group and transfection groups at 12 h, 24 h, 48 h were 0.25%, 12.57%, 17.29%, 15.03%, respectively. Compared with non-transfection group, the apoptotic rates of transfection groups increased significantly (Chi-square value was 7.357, 11.126 and 9.943 respectively, P < 0.01). The average optical density (AOD) of Bcl-2 protein in A549 cells in non-transfection group and transfection groups at 12 h, 24 h, 48 h were 2.02±0.07, 1.79±0.02, 1.25±0.51 and 1.21±0.24 respectively. Compared with non-transfection group, AOD of Bcl-2 protein in A549 cells in transfection groups decreased significantly (t value was 6.651, 7.089 and 7.438 respectively, P < 0.01). On the other hand, Bax protein expression in transfection groups increased, the AODs of Bax were 4.49±0.61, 4.24±0.37 and 3.95±0.43, respectively. Compared with non-transfection group (3.12±0.42), AOD of Bax protein in A549 celle in transfection groups increased significantly (t value was 7.469, 7.287 and 6.473 respectively, P < 0.01). In the Ad-Gax transfection groups the lower Bcl-2/Bax ratio was, the higher the apoptotic rate of A549 cells was (r=-0.49, P < 0.01). CONCLUSIONS: Ad-Gax transfection can induce A549 cells apoptosis. Possible mechanism is that Gax can downregulate Bcl-2 protein expression and upregulate Bax protein expression, and A549 cells apoptosis is related to the Bcl-2/Bax ratio.

[Effects of Gax gene transfection on proliferation and expression of proto-oncogenes in A549 cells].

BACKGROUND: Lung cancer is the leading cancer of malignant tumor in China.It is the direction that poeple make efforts to seek gene therapy of lung cancer. The aim of this study is to explore the effects of transfected growth arrest-specific homeobox gene (Gax gene) on the proliferation and expressions of c-fos and c-jun mRNA in A549 cells. METHODS: A549 cells were transfected with Gax gene by adenovirus. Expressions of Gax mRNA and protein were detected by RT-PCR and immunocytochemistry. The expressions of c-fos and c-jun mRNA were evaluated by RT-PCR. The proliferation inhibition effect of Gax transfection on A549 cells was evaluated by MTT assay. RESULTS: Only in the A549 cells transfected with Gax gene the Gax expression was confirmed by RT-PCR and immunocytochemistry. Compared with that in the control group, c-fos and c-jun mRNA level decreased significantly in Gax-transfected A549 cells (t=7.755, P < 0.01; t= 5.938 , P < 0.01). MTT assay showed that the proliferation inhibition rates of A549 cells transfected by Ad-Gax for 24h, 48h and 72h were (47.35±5.36)%, (54.96±1.78)%, and (65.39±5.11)% respectively. And these proliferation inhibition rates were significantly higher than those in the control group (Chi-Square=7.152, 9.431 and 12.847, P < 0.01). CONCLUSIONS: Gax gene can inhibit the proliferation of A549 cells. Its molecular mechanism may be through down-regulating the expressions of c-fos and c-jun.