[A clinicopathologic and prognosis study of Epstein-Barr virus positive diffuse large B-cell lymphoma in west-southern China].

OBJECTIVE: To investigate the clinicopathologic features, immunophenotype, and the prognosis related factors of Epstein-Barr virus (EBV) positive diffuse large B-cell lymphoma (DLBCL) in west-southern China. METHODS: There were 42 cases of EBV+ DLBCL in a total 586 DLBCL, the clinical and pathologic profiles of these patients were evaluated. Immunohistochemical study and in situ hybridization (ISH) of EBER1/2 were performed on formalin fixed tissues by tissue chips. The prognosis related factors were analyzed. RESULTS: The median age of these 42 EBV+ DLBCL patients was 62.5 years. The male-to-female ratio was 2.23 : 1. The site of occurrence included lymph node (69.05%) and spleen, stomach, tonsil, nasal cavity and nasopharynx. The mostly common initial clinical presentations were non-specific symptoms, such as lymphadenopathy, splenomegaly, hepatomegaly, fever, and fatigue. Morphologically, the majority (90.48%, 38/42) were pleomorphic subtypes and only 4 cases (9.52%) were simplex subtypes. Immunophenotype showed non-GCB type of DLBCL was predominance (83.33%, 35/42) by Hans classification. The expression of CD30, CD5, BCL-2, P53 and NF-kappaB/ P65 were 52.38% (22/42), 54.76% (23/42), 54.76% (23/42), 87.5% (35/40) and 0% (0/40) respectively. Follow-up data was available in 23 (54.76%) patients, 14 (60.87%) patients died of the tumor. 5-years overall survival was 16.5%. The median survival time was 40 months. The expression of BCL-2, increased LDH level and starry-sky morphologic character were associated with a poor prognosis. CONCLUSION: EBV positive DLBCL is not uncommon. Most lesions locate in lymph nodes. Pleomorphic histologic subtype is predominant. The tumor has worse prognosis with increased LDH level, starry-sky morphologic character and BCL-2 expression.

[An analysis of the clinicopathological features and misdiagnosis of 16 adults pulmonary sequestration].

OBJECTIVE: To explore the clinicopathological features of adult pulmonary sequestration and summarize the misdiagnosis experiences. METHODS: Data of 16 cases of adult pulmonary sequestration (18 years), who were confirmed by surgery and biopsy in our hospital were collected and reviewed. RESULTS: The median age of all the patients was 38.5 years. The female seemed to be more likely to suffer from adult pulmonary sequestration (n = 12) with cough to be the most frequent symptom (n = 9). CT scans revealed most of the lesions were located in the left lower lobes of the lungs (n = 9). Half of the lesions were characterized by pulmonary cyst-like changes and/or multiple cystic bronchiectasis (n = 8), followed by soft tissue mass in or out of the lung fields (n = 7). Enhanced CT scans showed abnormal arteries from the systemic circulation. Only two cases were diagnosed as pulmonary sequestration correctly in the primary diagnosis. The remaining were mostly misdiagnosed as pulmonary cyst-like changes with bronchiectasis (n = 6) or tumors (n = 6). According to the findings during surgery, 13 cases were intralobar pulmonary sequestrations; 3 cases were extralobars, whose tissues were all detected dysplasia and chronic inflammatory by histopathological examinations. CONCLUSIONS: The misdiagnosis rate of pulmonary sequestration is high because of its non-specific clinical symptoms. Since it is characterized by abnormal arteries and pulmonary dysplasia, enhanced CT scans should be used as a preferred screening method for suspected cases, especially for those middleaged patients with cystic or mass-like lesions in the left lower lobes of the lungs.

Role of chymase in cigarette smoke-induced pulmonary artery remodeling and pulmonary hypertension in hamsters.

BACKGROUND: Cigarette smoking is an important risk factor for pulmonary arterial hypertension (PAH) in chronic obstructive pulmonary disease (COPD). Chymase has been shown to function in the enzymatic production of angiotensin II (AngII) and the activation of transforming growth factor (TGF)-beta1 in the cardiovascular system. The aim of this study was to determine the potential role of chymase in cigarette smoke-induced pulmonary artery remodeling and PAH. METHODS: Hamsters were exposed to cigarette smoke; after 4 months, lung morphology and tissue biochemical changes were examined using immunohistochemistry, Western blotting, radioimmunoassay and reverse-transcription polymerase chain reaction. RESULTS: Our results show that chronic cigarette smoke exposure significantly induced elevation of right ventricular systolic pressures (RVSP) and medial hypertrophy of pulmonary arterioles in hamsters, concurrent with an increase of chymase activity and synthesis in the lung. Elevated Ang II levels and enhanced TGF-beta1/Smad signaling activation were also observed in smoke-exposed lungs. Chymase inhibition with chymostatin reduced the cigarette smoke-induced increase in chymase activity and Ang II concentration in the lung, and attenuated the RVSP elevation and the remodeling of pulmonary arterioles. Chymostatin did not affect angiotensin converting enzyme (ACE) activity in hamster lungs. CONCLUSIONS: These results suggest that chronic cigarette smoke exposure can increase chymase activity and expression in hamster lungs. The capability of activated chymase to induce Ang II formation and TGF-beta1 signaling may be part of the mechanism for smoking-induced pulmonary vascular remodeling. Thus, our study implies that blockade of chymase might provide benefits to PAH smokers.

[Expression and significance of MIF and CD147 in non-small cell lung cancer].

OBJECTIVE: To investigate the expression of macrophage migration inhibitory factor (MIF) and extracellular matrix metalloproteinase inducer (CD147) in non-small cell lung cancer (NSCLC) and its metastatic lymph node with tissue microarray technique, and to reveal clinical significance of these two molecules expression in NSCLC. METHODS: MIF and CD147 proteins were detected in 40 cases of benign pulmonary tissues, 327 cases of primary NSCLC and 112 cases of lymph node metastatic tissues by SP method of immunohistochemical staining. RESULTS: The expression of both MIF and CD147 in benign pulmonary tissues, NSCLC primary foci and metastatic lymph node appeared upward tendency (P < 0.05). Furthermore, expression level of MIF and CD147 proteins in NSCLC were related to the metastasis (P < 0.05) and TNM staging (P < 0.05). The Spearman correlation analysis showed that the expression of MIF and CD147 was positively correlated (r = 0.400, P = 0.000). Kaplan-Meier survival analysis indicated that the survival rate was markedly lower in patients with high expression level of MIF or CD147 than those with low expression level (P < 0.05). Multivariate analysis using Cox regression model identified that pathologic grading, metastasis, TNM staging and CD147 expression were independent prognostic factors of NSCLC patients (P < 0.05). CONCLUSION: MIF and CD147 may play important roles in invasion and metastasis in NSCLC, so might be employed to evaluate the prognosis of NSCLC patients.

[Expressions of APC and c-Myc and its implication on non-small cell lung cancer].

OBJECTIVE: To investigate the expressions of adenomatous polyposis coli (APC) protein and c-Myc protein in non-small cell lung cancer (NSCLC) and their lymph node metastases. METHODS: APC and c-Myc proteins were detected in 270 cases of primary NSCLC, 55 cases of lymph node metastatic tissues and 46 cases of adjacent normal lung tissues by EliVision and EnVision methods of immunohistochemical staining. RESULTS: Higher rates of the expressions of both APC and c-Myc proteins in NSCLC primary foci were found compared with those in lymph node metastases (P < 0.05). Furthermore, the expressions of APC and c-Myc proteins varied with histological types, TNM stagings and metastasis of the NSCLC (P < 0.05). The Spearman correlation analysis showed that the expressions of APC and c-Myc proteins were positively correlated (r(s) = 0.376, P = 0.000). The Kaplan-Meier survival analysis revealed that the survival rate was lower in patients with positive expressions of APC and c-Myc proteins than in patients with negative expressions (P < 0.05). Histological type, pathologic grading, metastasis and c-Myc were identified as independent risk factors with related to the prognosis of NSCLC patients in the multivariate Cox regression model (P < 0.05). CONCLUSION: APC and c-Myc may play an important role in the progression of NSCLC.

Blockade of advanced glycation end product formation attenuates bleomycin-induced pulmonary fibrosis in rats.

BACKGROUND: Advanced glycation end products (AGEs) have been proposed to be involved in pulmonary fibrosis, but its role in this process has not been fully understood. To investigate the role of AGE formation in pulmonary fibrosis, we used a bleomycin (BLM)-stimulated rat model treated with aminoguanidine (AG), a crosslink inhibitor of AGE formation. METHODS: Rats were intratracheally instilled with BLM (5 mg/kg) and orally administered with AG (40, 80, 120 mg/kg) once daily for two weeks. AGEs level in lung tissue was determined by ELISA and pulmonary fibrosis was evaluated by Ashcroft score and hydroxyproline assay. The expression of heat shock protein 47 (HSP47), a collagen specific molecular chaperone, was measured with RT-PCR and Western blot. Moreover, TGFbeta1 and its downstream Smad proteins were analyzed by Western blot. RESULTS: AGEs level in rat lungs, as well as lung hydroxyproline content and Ashcroft score, was significantly enhanced by BLM stimulation, which was abrogated by AG treatment. BLM significantly increased the expression of HSP47 mRNA and protein in lung tissues, and AG treatment markedly decreased BLM-induced HSP47 expression in a dose-dependent manner (p < 0.05). In addition, AG dose-dependently downregulated BLM-stimulated overexpressions of TGFbeta1, phosphorylated (p)-Smad2 and p-Smad3 protein in lung tissues. CONCLUSION: These findings suggest AGE formation may participate in the process of BLM-induced pulmonary fibrosis, and blockade of AGE formation by AG treatment attenuates BLM-induced pulmonary fibrosis in rats, which is implicated in inhibition of HSP47 expression and TGFbeta/Smads signaling.

VEGFR-2 antagonist SU5416 attenuates bleomycin-induced pulmonary fibrosis in mice.

OBJECTIVE: Abnormal angiogenesis is a central hallmark for the development and progression of idiopathic pulmonary fibrosis. It has been shown that vascular endothelial growth factor (VEGF) is one of the critical angiogenic factors in angiogenesis. The aim of the present study was to assess whether disruption of VEGF pathway would attenuate bleomycin-induced pulmonary fibrosis. METHODS: Bleomycin-induced pulmonary fibrosis mice were treated intraperitoneally with VEGF receptor tyrosine kinase inhibitor SU5416 at different phases after bleomycin infusion. We measured angiogenesis and inflammatory response in both bleomycin-treated and control mice, and correlated these levels with pulmonary fibrosis. RESULTS: The increased expressions of VEGF/VEGFR (Flk-1) were correlated to a larger number of microvessels and a higher score of pulmonary fibrosis. Early administration of SU5416 inhibited pulmonary collagen deposition, histopathologic fibroplasias and the activation of TGF-beta1/Smad3 signaling pathway in bleomycin-stimulated lung. These were also paralleled by a reduction of VEGF/VEGFR-2 (Flk-1) expression and microvessel numbers in lung. Furthermore, SU5416 inhibited inflammatory cell numbers and LDH activity in BALF and IL-13 expression in lung tissue at early inflammatory phase of bleomycin-induced pulmonary fibrosis. CONCLUSION: These results suggest that the VEGFR-2 inhibitor, SU5416, attenuates histopathologic fibroplasias and collagen deposition by regulating angiogenesis and inflammation in the lung.

Chronic infection of a seminal vesicle cyst as depicted on MR imaging.

Chronic infection of a seminal vesicle cyst is an extremely rare disorder worldwide. To date, only two cases, which were diagnosed initially by the use of contrast-enhanced CT or non-enhanced MR imaging, have been reported in the literature. We report here a case of a 78-year-old man with chronic infection of a seminal vesicle cyst to illustrate the usefulness of the pelvic contrast-enhanced MRI in making a definitive diagnosis of the rare disorder. In addition, a brief review of the relevant literature is presented.

[Intravascular large B-cell lymphoma: report of two autopsy cases with literature review].

OBJECTIVE: To study the clinicopathologic features of intravascular large B-cell lymphoma (IVLBCL). METHODS: Two autopsy cases of IVLBCL were retrieved from the archival file. The clinicopathologic features, immunohistochemistry and molecular findings were studied. RESULTS: The deceased were 70-year-old and 50-year-old males. Both of them had complained of a sudden onset of weakness and numbness of lower extremities. The clinical course deteriorated rapidly, with multi-organ failure. They died 85 days and 44 days after the presentation, respectively. Post-mortem examination did not reveal any mass lesion, except the presence of multiple skin and epicardium nodules, ranging from 0.5 cm to 2.5 cm in diameter, in the first patient. Pericardial effusion, ascites and pleural effusion were also observed. Histologically, neoplastic lymphoid cells filled up the small vessel lumina in many organs, including brain, hypophysis, spinal cord, spinal nerve roots, heart, lungs, kidneys, liver, spleen, digestive tract, pancreas, adrenal, thyroid, testes and lymph nodes. The tumor cells were relatively monotonous and of medium to large in size with round vesicular nuclei and 1 to 3 small basophilic nucleoli. Immunohistochemical study showed that the lymphoma cells expressed B-cell markers CD20 and CD79a, occasionally positive for CD5 and bcl-2 but negative for CD3, bcl-6, CD10, CD30, myeloperoxidase and cytokeratin. In-situ hybridization for Epstein-Barr virus-encoded RNA was negative. The proliferative index, as demonstrated by Ki-67 staining, was about 80%. Molecular study showed the presence of immunoglobulin heavy chain gene rearrangement in both cases, T-cell receptor-gamma gene rearrangement was not found. CONCLUSIONS: IVLBCL may present as neurological disturbance and carries distinctive morphologic characteristics, immunophenotype and molecular findings. The prognosis of this disease is often dismal.

[Non-small cell lung cancer evaluated by first pass dynamic contrast-enhanced 16-slice spiral CT: correlation of tumor vascularity with pathological characteristics].

OBJECTIVE: To investigate the role of first pass dynamic 16-slice spiral computed tomography in the evaluation of tumor angiogenesis in patients with non-small cell lung cancer (NSCLC) and to assess its importance in predicting pathologic characteristics. METHODS: The first pass dynamic 16-slice spiral computed tomography was performed in 33 patients with NSCLC. Their peak heights (PH) were measured with dynamic evaluation software. Their angiogenesis were labelled by anti-CD34 monoclonal antibody. The first pass peak heights (PH) in 33 patients with NSCLC were compared with their microvessel densities (MVD) and their relationships were assessed by linear regression analysis. RESULTS: Among the 33 patients with NSCLCs, the mean first pass PH and MVD of N1-2 were significantly higher than those at stage No (P < 0.01). The first pass PH of 33 NSCLC was correlated positively with MVDs. To differentiate stage N0 from stage N1-2 with 12 HU cutoff value of the first pass PH, the sensitivity, specificity, accuracy, positive predictive value and negative predictive value were 88.0%, 75.0%, 84.8%, 91.7% and 66.7%, respectively. CONCLUSION: The first pass dynamic contrast enhanced CT may be a predictor of tumor angiogenesis in patients with NSCLC and its pathologic characteristics, and may be helpful to improve the accuracy of lymph node staging with conventional CT.

[Expression of Merlin in cortex of temporal lobe and in hippocampal CA1 region of the Kindling Model of Epilepsy induced by corciaria lactone in rats].

OBJECTIVE: To explore the relationship between merlin and hippocampal sclerosis of temporal epilepsy. METHODS: The kindling model of epilepsy induced by corciaria lactone (CL) in rats was used. The expression of merlin in neuron of cortex of temporal lobe and hippocampal CA1 region was observed using immunohistochemistry method. Comparison of the amount of neuron with expression of merlin in the two locations was made between the kindled group, non-kindled group and control group. RESULTS: The expression of merlin in neuron of cortex of temporal lobe and hippocampal CA1 region of the kindled group was higher than the expression of the other two groups (P < 0.05), and there was no significant difference between the expression in the non-kindled group and that in the control group (P > 0.05). The expression of merlin in glial cell of the same region of all groups was seldom seen. CONCLUSION: The super-expression of merlin in neuron of cortex of temporal lobe and hippocampal CA1 region of the kindled rats may be involved in the process of neuronal apoptosis and hippocampal sclerosis.

[Expression of metabotropic glutamate receptor 1alpha in different brain areas of the kindled epilepsia models of rats by Coriaria lactone].

OBJECTIVE: To detect the expression of Metabotropic Glutamate Receptor 1alpha (MGLUR1alpha) in the different brain areas of the kindled epilepsia models of rats by Coriaria Lactone (CL). METHODS: Thirty male SD rats were divided into 3 groups and were given intramuscular injections of 0.75, 1.0 and 1.25 ml/kg Coriaria Lactone respectively. 5 rats in the control group were given intramuscular injection of 1.0 ml/kg saline. After the kindling models were completed, the EcoG of all groups were recorded with the multi-electrophysiology recorder to view whether the EcoG of kindled rats accord with their seizures and to know whether there are differencees in EcoG among the kindled, non-kindled and control groups. The coronary sections of brain tissue were HE stained and MGLUR1alpha immunohistochemistry stained, and were observed under light microscope. RESULTS: The kindled rats had all grade (Simialowski scale) seizures after CL injection and their seizures accorded with their EcoG features. The MGLUR1alpha expression of kindled rats in hippocampus and temporal cortex outside hippocampus was stronger than that of non-kindled and control rats (P < 0.05); the strong expression was noted to be of no obvious difference between neuron and glia. CONCLUSION: The MGLUR1alpha expression of kindled rats in hippocampus and temporal cortex outside hippocampus is stronger than that of non-kindled and control. It is possible that MGLUR1alpha participates in epileptic seizures.

Primary small cell carcinoma of esophagus: report of 9 cases and review of literature.

AIM: To analyze the clinical manifestations, pathological features and treatment of primary small cell carcinoma (SCC) of the esophagus and to review the literature on this entity. METHODS: The records of 9 patients with primary esophageal small cell carcinoma were examined and the demographic data, presenting symptoms, methods of tumor diagnosis, and types of treatment given, response to treatment, pathologic findings, and clinical outcome were reviewed. Features of mixed patterns of histological differentiation and lymph node metastases were specifically sought. RESULTS: All the patients reported dysphagia, weight loss and chest pain as the initial symptoms. In 5 cases the tumors were located in the mid-esophagus, 3 cases in the lower third of the esophagus and 1 case in the upper third. The average length of esophageal involvement was 5 cm. They underwent radical resection, regional lymph node clearance and esophageal-stomach anastomosis in thorax or at neck. Two patients had a stage IIa disease, five had a stage IIb disease, and the other two had a stage III disease of International Union Contrele Cancer (UICC). All of them were histologically and immunohistochemically confirmed SCC of esophagus. Immunohistochemical staining for neuron-specific enolase (NSE), synaptophsin (Syn) and chromogranin A exhibited strong immunoreactivity in all specimens. Three of the nine resected specimens showed foci of squamous cell carcinoma in situ. Metastasis was present in 7 of 9 adjacent lymph nodes. All the patients survived the operations and made an uneventful postoperative recovery. They received adjuvant systemic chemotherapy and local radiation therapy after discharge. During follow-up, three patients developed multiple liver, brain, lung and bone metastases and died between 5 and 18 mo after the diagnosis. Three patients developed widespread metastasis disease and died between 18 and 37 mo after the diagnosis. There was no local tumor recurrence in these 6 patients. The other three patients were lost during follow-up. CONCLUSION: Primary small cell carcinoma of the esophagus is a rare but very malignant tumor. Radical resection combined with chemotherapy and radiotherapy is helpful in limited stage cases.

[Expression and clinical significance of cyclooxygenase-2 in medulloblastoma].

OBJECTIVE: To gain an insight into the possible relationship between the expression of cyclooxygenase-2 (COX-2) and the prognosis of the patients with medulloblastoma. METHODS: COX-2 expression was investigated in 52 medulloblastoma and 10 normal cerebellar tissue specimens by immunohistochemistry. Kaplan-Meier analyses, Log-rank test, and Cox proportional hazard model were used to explore the relationship between the percentage of COX-2 expression and the survival period of patients with medulloblastoma. RESULTS: Positive staining with COX-2 was either moderately or strongly observed in most of the medulloblastoma (51/52). Moreover, COX-2 was expressed not only in tumor cells, but also in the vascular endothelial cells of tumor. No COX-2 immunoreactivity was observed in normal cerebellar tissue. Kaplan-Meier analyses demonstrated that high COX-2 expression (> or = 50% of cells stained positive) correlated with poor survival for the study group as a whole (P < 0.0001). CONCLUSION: Our study provides evidence that COX-2 is expressed in the majority of medulloblastomas and that a potential role of COX-2 inhibitors as an adjuvant therapy for brain tumors may exist.

Thymic epithelial tumors: a clinicopathologic study of 249 cases from a single institution.

The WHO histological classification for thymic epithelial tumors of 2004 edition is widely used, but its prognostic value is still controversial. In the present study we collected 249 Chinese patients with thymic epithelial tumors from West China Hospital of Sichuan University since 1999-2009 to assess the prognosis relating to tumor stages, histological classifications, MG and adjuvant therapy. There were 18 cases of type A (7.2%), 97 of type AB (39.0%), 22 of type B1 (8.8%), 63 of type B2 (25.3%), 16 of type B3 (6.5%) thymomas and 33 of thymic carcinomas (13.3%). According to the Massaoka staging, there were 107 patients in stage I (43%), 73 patients in stage II (29.3%), 50 patients in stage III (20.1%) and 19 in stage IV (7.6%). 101 patients (40.6%) complicated with MG, the incidence of MG was highest in type B3 thymomas, then in B2, none of thymic carcinomas complicated with MG. Cox regression analysis showed the Masaoka stage was the most important prognostic factor. Besides of staging, WHO histological classification was also an independent prognostic factor. The age, gender, MG and adjuvant therapy have no significant influence to the prognosis of the patients.

Toll-like receptor 4 relates to lipopolysaccharide-induced mucus hypersecretion in rat airway.

BACKGROUND: Toll-like receptor 4 (TLR4) is a transmembrane protein that participates in the recognition of lipopolysaccharide (LPS), a potentially important source of inflammation. To investigate the role of TLR4 in LPS-induced airway mucus hypersecretion (AMH), we used a LPS-induced rat model treated with dexamethasone (DEX). METHODS: Rats were randomly divided into four experimental groups: 1) saline (SA)-treated with distilled water (DW) (control group); 2) LPS-treated with DW (LPS group); 3) LPS-treated with DEX (LPS plus DEX group); 4) SA-treated with DEX (DEX group). DEX (5 mg/kg) was intraperitoneally injected 1 h before being administered intratracheally with LPS. Expressions of TLR4 and MUC5AC were evaluated with RT-PCR, in situ hybridization, immunohistochemistry and Alcian blue/Periodic acid-schiff (AB/PAS) staining. RESULTS: Increased expressions of TLR4 protein and mRNA were found in rat airway treated with LPS and peaked on day 2 after LPS administration. Following this, LPS increased MUC5AC expression and AB/PAS-stained goblet cells in rat airway. Correlation analysis showed TLR4 correlated well with the expression of MUC5AC (r = 0.684, p <0.01) and AB/PAS-stained area (r = 0.781, p <0.01). In addition, DEX pretreatment significantly reduced LPS-induced overexpression of TLR4 (p <0.05) in rat airway. CONCLUSIONS: These results suggest TLR4 relates to LPS-induced AMH and support a role of TLR4 in DEX inhibition of LPS-induced AMH.

Rosiglitazone, a peroxisome proliferator-activated receptor-gamma agonist, attenuates acrolein-induced airway mucus hypersecretion in rats.

BACKGROUND: Peroxisome proliferator-activated receptor-gamma (PPAR-gamma), a member of the ligand-activated nuclear receptor superfamily, has been shown to be implicated in anti-inflammatory and immunomodulatory responses, but its role in airway mucus hypersecretion remains not clear. OBJECTIVE: To investigate the role of PPAR-gamma in airway mucus hypersecretion, we used an acrolein-exposed rat model treated with rosiglitazone, a peroxisome proliferator-activated receptor-gamma agonist. METHODS: Rats were exposed to acrolein (3.0 ppm, 6h/day, 7 days/week) and orally administered with rosiglitazone (2, 4, 8 mg/kg) once daily for up to 2 weeks. The expressions of Muc5ac protein and mRNA, and infiltration of inflammatory cells and levels of inflammatory cytokines (interleukin (IL)-1beta, IL-8 and tumor necrosis factor (TNF)-alpha) in bronchoalveolar lavage fluid (BALF) were detected with real-time PCR, Western blot, cell counting and ELISA. In addition, the role of nuclear factor (NF)-kappaB pathway in this process was also explored. RESULTS: Acrolein exposure significantly induced goblet cell hyperplasia in bronchial epithelium and Muc5ac mRNA and protein expressions in rat lungs, as well as the associated airway inflammation evidenced by the increased numbers of inflammatory cells and levels of inflammatory cytokines in BALF, which were attenuated with rosiglitazone treatment in a dose-dependent manner (P<0.05). Simultaneously, the increased expression of NF-kappaB and decreased expression of cytoplasmic IkappaB in acrolein-exposed lungs were reversed by rosiglitazone treatment. CONCLUSIONS: These findings suggest that PPAR-gamma activation by its ligands can attenuate acrolein-induced airway mucus hypersecretion in rats, which may be involved in inhibition of NF-kappaB pathway.

[Expressions of Nm23, E-cadherin, and beta-catenin in non-small cell lung cancer and their correlations with metastasis and prognosis].

BACKGROUND & OBJECTIVE: Recently, studies showed nm23, E-cadherin, and Catenins play important roles in cellular signal transduction, which enhance complexity of their functions in tumor metastasis and can partly explain the diversity of the results from different studies. This study was to investigate correlations of expressions of nm23, E-cadherin, and beta-Catenin in non-small cell lung cancer (NSCLC) to metastasis and prognosis, and their interrelations. METHODS: Expressions of nm23, E-cadherin, and beta-Catenin in 112 specimens of NSCLC and 30 specimens of benign pulmonary lesion were detected by SP immunohistochemistry. RESULTS: The expressions of nm23, E-cadherin and beta-Catenin were significantly weaker in NSCLC tissues than in adjacent non-cancerous tissues, and benign pulmonary tissues (53.0% vs. 64.8%, and 76.9%, P < 0.01; 53.1% vs. 79.7%, and 83.5%, P < 0.01; and 47.2% vs. 80.6%, and 85.6%, P < 0.01), significantly weaker in NSCLC tissues with lymph node metastasis than in those without metastasis (48.0% vs. 65.0%, P < 0.01; 47.3% vs. 60.5%, P < 0.01; and 41.8% vs. 60.3%, P < 0.01), and significantly weaker in NSCLC tissues of stage III-IV than in those of stage I-II (44.8% vs. 67.2%, P < 0.01; 46.6% vs. 64.3%, P < 0.01; 38.1% vs. 63.1%, P < 0.01). The 5-year survival rates of patients with weak expressions of nm23, E-cadherin, and beta-Catenin were significantly lower than those of patients with strong expressions (3.6% vs. 39.3%, P < 0.01; 6.8% vs. 35.8%, P < 0.01; and 3.8% vs. 37.3%, P < 0.01). CONCLUSIONS: Down-regulations of nm23, E-cadherin, and beta-catenin closely relate to metastasis of NSCLC. Detection of nm23, E-cadherin, and beta-Catenin might be helpful to predict prognosis of NSCLC patients.