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Background Long non-coding RNAs (lncRNAs) have been uncovered to be essential regulators in the biological processes of human cancers, including lung adenocarcinoma (LUAD). Recently, small nucleolar RNA host gene 17 (SNHG17) has been identified as one novel oncogenic lncRNA in gastric cancer. However, it remains unclear whether SNHG7 exert functions in LUAD progression. Methods The expression levels of SNHG17, miR-485–5p and Wnt ligand secretion mediator (WLS) in LUAD cells was evaluated by RT-qPCR. The effect of SNHG7 silencing on LUAD cell proliferation was assessed by colony formation and EdU assays. The apoptosis of LUAD cells was measured by flow cytometry analysis. Transwell assays were applied to detect cell migration and invasion. The relationship between SNHG17 and miR-485–5p was validated by RIP, RNA pull down and luciferase reporter assays. Results SNHG17 and WLS were up-regulated in LUAD cell lines. Down-regulation of SNHG17 curbed LUAD cell proliferation, migration and invasion but facilitated apoptosis. SNHG17 acted as miR-485–5p sponge to upregulate WLS expression. Conclusion SNHG17 triggers the progression of LUAD via sponging miR-485–5p to upregulate WLS expression.

To analyze clinical characteristics and risk factors for in-hospital mortality in patients coinfected with P. jirovecii and Aspergillus.This study included 53 patients with coinfection of P. jirovecii pneumonia (PJP) and invasive pulmonary aspergillosis (IPA) in our center from January 2011 to December 2021. All cases were divided into survivor (n=27) and non-survivor groups (n=26). Medical records, laboratory and radiology data were collected. Risk factors for in-hospital mortality were identified by multivariable analyses.HIV-positive patients accounted for 3.8%. Fever (77.4%), dyspnea (69.8%) and wet cough (24.5%) were common symptoms. Ground-glass opacity (83.0%), consolidation (71.7%), septal thickening (66.0%), and nodules (54.7%) were the most common radiological signs. CD4+ T cell count and serum albumin (ALB) level were significantly lower in non-survival group than in the survival group. Conversely, serum lactate dehydrogenase (LDH) and procalcitonin (PCT) levels were higher in non-survival group than in survival group. Lactic acidosis [odds ratio (OR): 33.999,95% confidential interval (CI): 3.112-371.409; p=0.004], low CD4+ T cell count (114 cell/µL) [OR: 19.343, 95% CI: 1.533-259.380; p=0.022] and high level of LDH (519 U/L) [OR: 11.422, 95% CI: 1.271-102.669; p=0.030] were independent risk factors for mortality.PJP coinfected with IPA incurs high mortality with nonspecific clinical characteristics and is more likely to involve HIV-negative patients. Lactic acidosis, low CD4+ T cell count and high LDH level are independent risk factors for mortality, close monitoring of these parameters is necessary to help distinguish high-risk patients and make appropriate clinical decisions.

Purpose LINC00680 was reported to be involved in various cancers through multiple mechanisms. Therefore, we intended to investigate its role in the progression of non-small cell lung cancer (NSCLC). Materials and methods Firstly, quantitative real-time polymerase chain reaction (qRT-PCR) was used to test LINC00680 in NSCLC tissue and cell lines. Subsequently, A549 and H1299 cells were transfected with LINC00680 overexpressing plasmids and their proliferation and colony formation and apoptosis was tested by Transwell assay and flow cytometry. In addition, xenograft tumor experiments in nude mice also affirmed. Meanwhile, we predicted that miR-410-3p, LINC00680 and high-mobility group protein box 1(HMGB1) relationship by Starbase, dual-luciferase reporter and RIP assay. Finally, the carcinogenic effects of LINC00680 were reversed by ethyl pyruvate (EP), a specific inhibitor of HMGB1. Results LINC00680 was upregulated in NSCLC and was closely related to the malignancy and poor prognosis of NSCLC patients. LINC00680 promoted proliferation and colony formation and inhibited apoptosis of A549 and H1299 cells. In addition, overexpressing LINC00680 accelerated the growth of NSCLC cells in xenograft tumor experiments in nude mice also affirmed. Meanwhile, high-mobility group protein box 1(HMGB1) was astoundingly amplified in NSCLC and was negatively regulated by miR-410-3p. Further, HMGB1 acted as a downstream target of miR-410-3p, upregulating miR-410-3p to attenuate HMGB1, while LINC00680 strengthened the expression of HMGB1 in A549 and H1299 cells. Discussion Thus, these results indicated that LINC00680 was cancerogenic in NSCLC by upregulating HMGB1 via sponging miR-410-3p.

Eosinophilic asthma (EA) is one of the most important asthma phenotypes with distinct features. However, its genetic characteristics are not fully understood. This study aimed to investigate the transcriptome features and to identify hub genes of EA. Differentially expressed genes (DEGs) analysis, weighted gene coexpression network analysis (WGCNA) and protein–protein interaction (PPI) network analysis were performed to construct gene networks and to identify hub genes. Enrichment analyses were performed to investigate the biological processes, pathways and immune status of EA. The hub genes were validated in another dataset. The diagnostic value of the identified hub genes was assessed by receiver operator characteristic curve (ROC) analysis. Compared with NEA, EA had a different gene expression pattern, in which 81 genes were differentially expressed. WGCNA identified two gene modules significantly associated with EA. Intersections of the DEGs and the genes in the modules associated with EA were mainly enriched in chemotaxis and signal transduction by GO and KEGG enrichment analyses. Single-sample gene set enrichment analysis (ssGSEA) indicated that EA had different immune infiltration and functions compared with NEA. Seven hub genes of EA were identified and validated, including CCL17, CCL26, CD1C, CXCL11, CXCL10, CCL22, and CCR7, all of which have diagnostic values for distinguishing EA from NEA (All AUC > 0.7). This study demonstrated the distinct gene expression patterns, biological processes, and immune status of EA. Hub genes of EA were identified and validated. Our study could provide a framework of co-expression gene modules and potential therapeutic targets for EA.

Circular RNAs (circRNAs) have recently been described as key regulators in the progression of non-small cell lung cancer (NSCLC), and this study aimed to investigate the functional role of circMAT2B in NSCLC. CircMAT2B expression in NSCLC tissues and cell lines was investigated using RT-qPCR analysis. A series of functional experiments, including MTT assay, colony formation assay, wound healing assay and transwell assay, were carried out to investigate the effects of circMAT2B knockdown/overexpression on the malignant traits of NSCLC cells. Western blot analysis was performed to detect the expression of EMT-related proteins. Dual-luciferase reporter assay and RIP assay were further carried out to analyze the interaction between circMAT2B and miR-431 in NSCLC. We observed that circMAT2B was overexpressed in NSCLC tissues and cell lines, and high expression of circMAT2B was closely associated with large tumor size, advanced TNM stage and poor prognosis of NSCLC patients. Further functional experiments showed that circMAT2B knockdown markedly inhibited the proliferation, migration, invasion and EMT of NSCLC cells, whereas circMAT2B overexpression led to the opposing results. Mechanistically, circMAT2B could directly interact with miR-431, and subsequently decrease miR-431 expression in NSCLC. The effects of circMAT2B overexpression in NSCLC cells were abrogated by miR-431 restoration. Our findings revealed the novel oncogenic roles of circMAT2B in NSCLC by sponging miR-431.

Primary pulmonary lymphoepithelioma-like carcinoma (PPLELC) is a rare subtype of non-small cell lung cancer (NSCLC) for which there is currently no recognized treatment. Recently, favorable immune checkpoint blockade responses have been observed in PPLELC. This study aimed to review the effects of this regimen in patients with advanced PPLELC. PPLELC patients treated with immune checkpoint inhibitors at West China Hospital between January 2008 and December 2019 were retrospectively identified. Demographic parameters and antitumor treatment details were retrieved and reviewed. Among 128 patients diagnosed with PPLELC, 5 who received immune checkpoint inhibitors at advanced stages were included in the analysis. All of these patients were female nonsmokers with a median age of 55.6 (range 53-58) years at diagnosis. Their median PD-L1 expression was 40% (range, 30-80%). Although the patients underwent surgeries, chemotherapy and radiotherapy, all the treatments failed. Immune checkpoint inhibitors were administered palliatively, and three patients responded favorably, with the best overall response being partial remission (PR). Thus, immune checkpoint inhibitors may be a promising treatment for advanced PPLELC, and large clinical trials are warranted to obtain more evidence regarding this regimen.

Lung cancer is the leading cause of cancer death and there have been clinical prediction models. This study aimed to evaluate the diagnostic performance of published models and create new models to evaluate the probability of malignant solitary pulmonary nodules (SPNs) in Chinese population. We consecutively enrolled 2061 patients with SPNs from West China Hospital between January 2008 and December 2016, each SPN was pathologically confirmed. First, four published prediction models, Mayo clinic model, Veterans Affairs (VA) model, Brock model and People’s Hospital of Peking University (PEH) model were validated in our patients. Then, utilizing logistic regression, decision tree and random forest (RF), we developed three new models and internally validated them. Area under the receiver operating characteristic curve (AUC) values of four published models were as follows: Mayo 0.705 (95% CI 0.658–0.752, n = 726), VA 0.64 6 (95% CI 0.598–0.695, n = 800), Brock 0.575 (95% CI 0.502–0.648, n = 550) and PEH 0.675 (95% CI 0.627–0.723, n = 726). Logistic regression model, decision tree model and RF model were developed, AUC values of these models were 0.842 (95% CI 0.778–0.906), 0.734 (95% CI 0.647–0.821), 0.851 (95% CI 0.789–0.914), respectively. The four published lung cancer prediction models do not apply to our population, and we have established new models that can be used to predict the probability of malignant SPNs.

Purpose LINC00680 was reported to be involved in various cancers through multiple mechanisms. Therefore, we intended to investigate its role in the progression of non-small cell lung cancer (NSCLC). Materials and Methods Firstly, quantitative real-time polymerase chain reaction (qRT-PCR) was used to test LINC00680 in NSCLC tissue and cell lines. Subsequently, A549 and H1299 cells were transfected with LINC00680 overexpressing plasmids and their proliferation and colony formation and apoptosis was tested by Transwell assay and flow cytometry. In addition, xenograft tumor experiments in nude mice also affirmed. Meanwhile, we predicted that miR-410-3p, LINC00680 and high-mobility group protein box 1(HMGB1) relationship by Starbase, dual-luciferase reporter and RIP assay. Finally, the carcinogenic effects of LINC00680 were reversed by ethyl pyruvate (EP), a specific inhibitor of HMGB1. Results LINC00680 was upregulated in NSCLC and was closely related to the malignancy and poor prognosis of NSCLC patients. LINC00680 promoted proliferation and colony formation and inhibited apoptosis of A549 and H1299 cells. In addition, overexpressing LINC00680 accelerated the growth of NSCLC cells in xenograft tumor experiments in nude mice also affirmed. Meanwhile, high-mobility group protein box 1(HMGB1) was astoundingly amplified in NSCLC and was negatively regulated by miR-410-3p. Further, HMGB1 acted as a downstream target of miR-410-3p, upregulating miR-410-3p to attenuate HMGB1, while LINC00680 strengthened the expression of HMGB1 in A549 and H1299 cells. Discussion Thus, these results indicated that LINC00680 was cancerogenic in NSCLC by upregulating HMGB1 via sponging miR-410-3p.

Dasatinib is a tyrosine kinase inhibitor for the treatment of BCR-ABL-positive chronic myeloid leukaemia (CML) or Philadelphia chromosome-positive acute lymphoblastic leukaemia (ALL). Although fluid retention is a common adverse event associated with dasatinib, chylothorax is exceptionally rare. The pathological mechanism, clinical manifestation and management of dasatinib-induced chylothorax are completely unclear. A 71-year-old man treated with dasatinib for CML was admitted for progressive dyspnea. Computed tomography (CT) showed a pleural effusion that was more prominent on the right thoracic cavity. Thoracentesis showed thick milky pleural fluid, which was then confirmed as chylothorax by chylum qualitative tests and triglyceride measurements. Radionuclide lymphoscintigraphy yielded an obstruction at the end segment of the thoracic duct, but no leakage points were found. After excluding common causes, drug-induced chylothorax was presumed. Then, dasatinib was withdrawn, and 1 week later, chylothorax resolved. To further elucidate the relationship between the medication and chylothorax, dasatinib was resumed tentatively for 2 days. As expected, pleural effusion recurred soon. Based on these clinical manifestations, the diagnosis of dasatinib-induced chylothorax was identified. The patient was suggested to stop dasatinib and use an alternative drug as recommended by the haematologist. Pleural effusion is the common adverse reaction of dasatinib, but chylothorax is rare. Only six cases of dasatinib-induced chylothorax have been reported, and our patient is the seventh case. Once a patient with dasatinib treatment develops chylothorax, dasatinib should be considered one of the possible causes. If no other definitive aetiological factor is identified, dasatinib discontinuation might be the optimum scheme.

Rationale: Acute fibrinous and organizing pneumonia (AFOP) is a newly evolving rare non-infectious lung pathology, characterized by intra-alveolar fibrin balls on histology. It is usually difficult to be diagnosed and mistaken for other lung diseases. Patient concerns: In this article, an interesting case about a male patient with a 15-day history of high-grade fever, chills, and no productive cough was presented. He was misdiagnosed as the lung infection early, but exhibited no response to the antibiotic therapy. Diagnosis: The diagnosis of AFOP was determined by the lung biopsy and pathology. Interventions: With the diagnosis of AFOP, all antibiotics were discontinued, and 40 mg methylprednisolone daily was given intravenously. Outcomes: The patient responded well to the treatment with steroids. Lessons: AFOP is a rare lung disease characterized by bilateral basilar infiltrates and histological findings of organizing pneumonia and intra-alveolar fibrin in the form of “fibrin balls”. Lung biopsy and histopathology were the most important diagnostic methods for the AFOP. Glucocorticoid was an effective drug for the treatment. Subacute patients of AFOP have excellent prognosis with corticosteroids.

Background This meta-analysis aimed to systematically estimate the prevalence of comorbid bronchiectasis in patients with asthma and to summarize its clinical impact. Methods Embase, PubMed, and Cochrane Library electronic databases were searched to identify relevant studies published from inception until March 2020. Study selection Studies were included if bronchiectasis was identified by high-resolution computed tomography. Outcomes included the prevalence of bronchiectasis and its association with demographic characteristics and indicators of asthma severity, including results of lung function tests and the number of exacerbations. Results Five observational studies with 839 patients were included. Overall, the mean prevalence of bronchiectasis in patients with asthma was 36.6% (307/839). Patients with comorbid bronchiectasis had lower forced expiratory volume in 1 second (FEV1)/forced vital capacity (FVC) (MD: -2.71; 95% CI: -3.72 to -1.69) and more frequent exacerbations (MD: 0.68; 95% CI: 0.03 to 1.33) than those with asthma alone, and there was no significant difference of sex, duration of asthma and serum levels of immunoglobulin(Ig)Es between asthmatic patients with or without bronchiectasis. Conclusion The presence of bronchiectasis in patients with asthma was associated with greater asthma severity. There are important therapeutic implications of identifying bronchiectasis in asthmatic patients.

Adenoid cystic carcinoma (ACC) is the second most common tracheal tumor, but its optimal treatment strategy is still controversial. To further elucidate the impact of treatment on disease-free survival (DFS) and overall survival (OS), we retrospectively investigated different treatment modalities and outcomes of 56 patients with primary ACC of the trachea treated at four hospitals in Sichuan Province of China from 1995 to 2012. 52 patients were included in the analysis. 4 patients with unresectable tumors were treated primarily with radiotherapy (RT) alone. 11 of 48 patients who received surgery as primary therapy obtained complete resection without adjuvant therapy. 24 of 37 patients who had incomplete resection (R1, R2) received postoperative RT while 13 patients were treated without postoperative RT. Postoperative chemotherapy (CT) was used in 12 patients with postoperative RT. No significant difference was shown in DFS (p = 0.683) and OS (p = 0.829) between patients with complete resection and those with incomplete resection. Postoperative RT for patients with incomplete resection was associated with improved DFS (92 vs. 62 months, p = 0.027) and OS (125 vs. 78 months, p = 0.004). Postoperative chemotherapy (CT) following RT did not have a significant impact on DFS (p = 0.390) or OS (p = 0.646) in patients with positive margin. These observations suggest that postoperative RT should probably be recommended for patients with incomplete resection. Postoperative CT following RT in patients with incomplete resection did not seem to produce an additional survival benefit.

A number of polymorphisms in a disintegrin and metalloprotease 33 (ADAM33) gene have been implicated in susceptibility to chronic obstructive pulmonary disease (COPD). However, results to date have been inconclusive. We conducted meta-analyses to investigate the associations between multiple polymorphisms in ADAM33 gene and COPD susceptibility. PubMed, Embase and Chinese databases (Wanfang and China National Knowledge Infrastructure) were searched for eligible case-control studies. We extracted data and used meta-analysis to calculate pooled odds ratios with 95% confidence intervals to evaluate the strength of associations. Twelve studies containing six ADAM33 polymorphisms (F+1, S1, S2, T1, V4 and Q-1) were identified, which involved 2630 cases and 4376 controls. ADAM33 S1 polymorphism showed stable and significant associations with COPD risks among the Chinese and smoking populations, and Q-1 polymorphism showed stable and significant associations with COPD risks among the overall populations. In subgroup analyses, T1 and Q-1 polymorphisms were significantly associated with COPD risks among the Chinese and smoking populations, and among the Chinese, Caucasians and smoking populations, respectively. However, none of the significant results was stable in sensitivity analyses. With respect to F+1, S2 or V4 polymorphism, there was no evidence of any significant association with COPD risks in either the overall or the subgroup analysis. The results of this meta-analysis indicate that ADAM33 S1 polymorphism is a risk factor for COPD among the Chinese and smoking populations, and that Q-1 polymorphism is a risk factor for COPD among the overall populations.

Quercetin is a herbal flavonoid derived from various foods of plant origin and widely used as a major constituent of nutritional supplements. Quercetin has been shown to have anti-inflammatory properties and can play a role in anti-inflammatory procedure. Intercellular adhesion molecule-1 (ICAM-1) is one of the important pro-inflammatory factors, especially in early phage of inflammation. However, the mechanisms regulating ICAM-1 expression by quercetin in human A549 cells were still unclear. In this study, the inhibitory effect of quercetin on ICAM-1 expression by interleukin-1 beta (IL-1 beta)-stimulated A549 cells was investigated, and the roles of mitogen-activated protein kinases (MAPK) pathways were explored. Quercetin attenuated IL-1 beta-induced expression of ICAM-1 mRNA and protein in a dose-dependent manner. The experiment suggested that quercetin actively inhibited inhibitory protein of nuclear factor-kappa B (I kappa B) degradation, and nuclear factor-kappa B (NF-kappa B) activity. The c-fos and c-jun, components of activator protein-1 (AP-1), were mediated by MAPK pathways. ERK and p38 were involved in the c-fos mRNA expression, and JNK was involved in the c-jun mRNA expression. The inhibitory effect of quercetin on ICAM-1 expression was mediated by the sequential attenuation of the c-fos and c-jun mRNA expressions. These inhibitory effects were partially inhibited by SB203580, a specific inhibitor of p38 MAPK, but not by PD98059, a specific inhibitors of extracellular signal-regulated kinase (ERK), and SP600125, a specific inhibitor of c-Jun-N-terminal kinase (JNK). Taken together, these results suggest that quercetin negatively modulating ICAM-1 partly dependent on MAPK pathways.

A number of polymorphisms in a disintegrin and metalloprotease 33 (ADAM33) gene have been implicated in susceptibility to chronic obstructive pulmonary disease (COPD). However, results to date have been inconclusive. We conducted meta-analyses to investigate the associations between multiple polymorphisms in ADAM33 gene and COPD susceptibility. PubMed, Embase and Chinese databases (Wanfang and China National Knowledge Infrastructure) were searched for eligible case-control studies. We extracted data and used meta-analysis to calculate pooled odds ratios with 95% confidence intervals to evaluate the strength of associations. Twelve studies containing six ADAM33 polymorphisms (F+1, S1, S2, T1, V4 and Q-1) were identified, which involved 2630 cases and 4376 controls. ADAM33 S1 polymorphism showed stable and significant associations with COPD risks among the Chinese and smoking populations, and Q-1 polymorphism showed stable and significant associations with COPD risks among the overall populations. In subgroup analyses, T1 and Q-1 polymorphisms were significantly associated with COPD risks among the Chinese and smoking populations, and among the Chinese, Caucasians and smoking populations, respectively. However, none of the significant results was stable in sensitivity analyses. With respect to F+1, S2 or V4 polymorphism, there was no evidence of any significant association with COPD risks in either the overall or the subgroup analysis. The results of this meta-analysis indicate that ADAM33 S1 polymorphism is a risk factor for COPD among the Chinese and smoking populations, and that Q-1 polymorphism is a risk factor for COPD among the overall populations.

There have been a lot of studies about surface adhesion molecule (CD44) in recent years, however study on osteopontin (OPN) is still few. The aim of this study is to investigate the levels of OPN and CD44v6 in lung cancer and their correlation.OPN and CD44v6 expression were detected in 78 lung cancer tissues by immunohistochemistry.The positive rate of OPN and CD44v6 expression in non-small cell lung cancer (NSCLC) was 58.46% and 66.15% respectively, but no positive case in small cell lung cancer. The expression of OPN and CD44v6 in NSCLC was closely related to TNM stages (P0.01), but not to cell differentiation (P0.05). There was a remarkably positive correlation between the expression of OPN and CD44v6 (r=0.255, P0.05).The co-expression of OPN and CD44v6 may be involved in progression and metastasis of lung cancer. The interrelationship of OPN and CD44v6 was coordinative with development and metastasis of lung cancer. It might be helpful to predict the metastasis and prognosis of NSCLC.

Mechanical force plays an important role in physiological function and pathophysiologic conditions of respiratory system. Recently, a number of researches focused on how mechanical force affected pulmonary cells. This paper reviews the molecular basis of mechanical force in detail. The significance of mechanical force in respiratory therapy is also discussed.

Background and objective: The pattern and the degree of mechanical stimuli may determine cellular responses, but little is known about how low magnitude stimuli are converted into biochemical signals in alveolar epithelial cells (AEC). The aim of this study was to explore whether extracellular signal-regulated kinases 1/2 (ERK1/2) are activated by low-level strain in A549 cells and how mechanical factors affect ERK1/2 phosphorylation. Methods: A549 cells (an AEC line) were exposed to cyclic tensile strain via a four-point bending system, with strains of different magnitude (437, 874, 1748, 3496 µstrain), duration (5, 15, 30, 60, 120 min) and frequency (0.5, 1 Hz). Phosphorylation of ERK1/2 proteins was assessed by western blot. Results: Maximal ERK1/2 phosphorylation occurred in the 874 µstrain group (a 2.25-fold increase, P

Background: Mechanicalventilation can affect the lung, causing edema and alveolar inflammation. Intercellular adhesion molecule-1 (ICAM-1) plays an important role in this inflammatory response. Objective: The aims of this study were to investigate whether cyclic cell stretch upregulates the production of ICAM-1 by human alveolar epithelium and to explore possible mechanisms of upregulation. Methods: Human type 2-like alveolar epithelial cells (A549 cells) were exposed to cyclic tensile strain via a four-point bending system, with strains of varying frequency (0.2, 0.5, and 1 Hz), duration (0, 1, 3, and 6 h), and magnitude (500, 1,000, and 2,000 microstrain). Strain was applied at varying frequency (0.2, 0.5, 1 Hz) but at constant time (3 h) and magnitude (1,000 microstrain), at varying duration (0, 1, 3, and 6 h) but at constant frequency (0.5 Hz) and magnitude (1,000 microstrain), or at varying magnitude (500, 1,000, and 2,000 microstrain) but at constant time (3 h) and frequency (0.5 Hz). Results: Mechanical loading induced ICAM-1 protein and mRNA production in a frequency- and duration-dependent manner. At the 3-hour time point, large loadings (1,000 or 2,000 microstrain) upregulated ICAM-1 protein production, but there was no statistically significant difference between these two groups (p > 0.05). PD98059, a specific inhibitor of extracellular signal-regulated kinase (ERK), and N-acetylcysteine (NAC), an antioxidant, partially abrogated the stretch-induced ICAM-1 protein upregulation at the 3-hour loading. Conclusion: Mechanical strain can upregulate ICAM-1 production. The response is frequency and duration dependent, which may involve both ERK pathways and reactive oxidant species production.

To investigate the role of adrenomedullin (AM) in the development of hypoxic pulmonary hypertension (HPH), and to assess the expression of AM and adrenomedullin receptor (AMR) in the lungs of rats with HPH.We exposed 10 rats to normobaric hypoxic conditions for 3 weeks to establish rat model of pulmonary hypertension; and 10 other rats were used as normoxic controls. Mean pulmonary arterial pressure (mPAP) was measured by a right cardiac catheterization. The thickness of pulmonary arterioles was measured by a computerized image analyzer. We used the reverse transcription-polymerase chain reaction (RT-PCR) to assess the change of expression of AM and AMR in lung of HPH rat model.Compared with the control group, hypoxic rats developed remarkable pulmonary hypertension, increment in the thickness of pulmonary arterioles and right ventricular hypertrophy (P0.01). Chronic hypoxia elicited a considerable increment in expression of AM and AMR in the lungs of rats, and the ratio of AM/beta-actin and AMR/beta-actin in lungs of rats treated with hypoxia were significantly higher (P0.01).The AM plays an important role in regulating pulmonary vascular tone and can ameliorate the development of hypoxic pulmonary hypertension in rats.

To investigate the prophylactic effect of BCG polysaccharides nucleic acid (BCG-PSN) on patients with chronic obstructive pulmonary disease and inquire about the mechanism thereof.Sixty patients with chronic obstructive pulmonary disease were divided into two groups. In the treatment group, 36 patients received BCG-PSN 0.5 mg intramuscular injection, quaque die alterna, for 18 times. All patients revisited the hospital every 2 weeks and were followed up for 6 months. The number and days of patients with acute attack in 3 and 6 months were assessed. In the treatment group, the blood samples were collected before treatment and 3 and 6 months after treatment for the measurement of the blood IgA, IgG, IgM, CD3, CD4 and CD8.The number and days of patients with acute attack in the treatment group were significantly lower than those in the control group. After the treatment by BCG-PSN, blood CD4 and CD4/CD8 were significantly increased.BCG-PSN increases the patient's cellular immunocompetence and thus serves as a good protection against the acute attack of chronic obstructive pulmonary disease.

To evaluate the effect of adrenomedullin (ADM) on pulmonary circulation and the change of ADM in plasma and lung tissue from rats with hypoxic pulmonary hypertension.Fifty Wistar rats were divided into the control group (10 rats) and the hypoxic group (40 rats). The animal model of pulmonary hypertension was established by exposing the rats to normobaric hypoxic conditions for 3 weeks; Mean pulmonary arterial pressure (mPAP) was measured by right cardiac catheterization, and mean systemic blood pressure (mSBP) was measured by left femoral catheterization. The thickness of pulmonary arterioles was measured by a computerized image analyser. The level of ADM in plasma and lung tissue was measured by radioimmunoassay. We ADM was administered in doses of 0.5, 1.0, 2.0 nmol/kg respectively to 30 hypoxic rats and the changes in mPAP and mSBP to ADM was evaluated.Rats exposed to hypoxia developed pulmonary hypertension, the mPAP in the control group being (16 +/- 3) mm Hg and in hypoxic group being (30 +/- 4) mm Hg, and the difference was significant (P0.01). The hypoxic rats developed significantly thickened pulmonary arterioles. The plasma level of ADM was (288 +/- 24) pg/ml in the hypoxic rats and (168 +/- 25) pg/ml in the control group the difference being significant (P0.01). The level of ADM in the lung homogenates from the hypoxic group was (2 319 +/- 238) pg/g and that from the control group was (1 153 +/- 127) pg/g and the difference was significant (P0.01). The ADM levels had a positive correlation with the mPAP (gamma = 0.567 and 0.612 P0.01, respectively). Administration of exogenous ADM reduced the mPAP in a dose-dependent manner in hypoxic rats, and the effect lasted 5 approximately 15 minutes.ADM has a relaxing effect on pulmonary circulation. The change of ADM in plasma and lung tissue may serve as a compensatory mechanism in maintaining the stability of pulmonary circulation in hypoxic condition.

To assess the effect of tetrandrine (Tet) pulmonary targeting microspheres on hypoxic pulmonary hypertension and evaluate its selective action on pulmonary circulation.Twenty rats were exposed to hypoxic conditions for 3 weeks. Ten rats were used as normoxic controls. We administered Tet pulmonary targeting microspheres to 10 hypoxic rats and Tet aqueous solution to 10 hypoxic rats and the 10 control rats. Mean pulmonary arterial pressure (mPAP) was measured by a right cardiac catheterization, and mean systemic blood pressure (mSBP) was measured by left femoral catheterization.Rats exposed to hypoxia developed pulmonary hypertension. The decrease in mPAP in rats treated with Tet pulmonary targeting microspheres was significantly greater than that in rats receiving Tet aqueous solution (P0.05), and the effects were longer with Tet pulmonary targeting microspheres. Moreover, Tet pulmonary targeting microspheres, unlike Tet aqueous solution, did not decrease mSBP.Tet pulmonary targeting microspheres were more effective than Tet aqueous solution treating hypoxic pulmonary hypertension and acted selectively on the pulmonary circulation.