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1. Chang YS, Chung JH, Shin DH, Chung KY, Kim YS, Chang J, Kim SK, Kim SK: Retinoic acid receptor-beta expression in stage I non-small cell lung cancer and adjacent normal appearing bronchial epithelium. Yonsei Med J; 2004 Jun 30;45(3):435-42
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  • [Title] Retinoic acid receptor-beta expression in stage I non-small cell lung cancer and adjacent normal appearing bronchial epithelium.
  • Retinoic acid receptor-beta (RAR-beta) is induced by and mediates the growth-inhibitory and apoptotic effects of retinoic acid (RA), suggesting that loss of RAR-beta expression may be one of the critical events involved in the carcinogenesis/ progression of non-small cell lung cancer (NSCLC) and in the responsiveness to retinoid chemotherapy.
  • However, recent contradictory reports that the expression of RAR-beta is associated with poor clinical outcome, and the fact that treatment of serum-deprived type 2 alveolar cells with RA leads to a stimulation of cell proliferation, require the verification of RAR-beta as a biomarker of chemoprevention or prognosis.
  • The expression status of RAR-beta in cancer cells and adjacent normal appearing bronchial epithelium from 39 patients, diagnosed as stage I NSCLC and undergone a curative lung resection, was analyzed in paraffin-embedded tissue sections by IHC staining.
  • The normal appearing bronchial epithelium of 14 out of 33 (42.4%) specimens expressed RAR-beta, whereas 22 out of the 39 (56.4%) stage I NSCLC specimens expressed RAR-beta.
  • Neither the expression status in normal appearing adjacent tissue nor that in the tumor tissue had prognostic implications.
  • The higher expression of RAR-beta in cancer tissue, the focal and uneven distribution in normal appearing adjacent bronchial epithelium, and inconsistency with the corresponding tumor tissue, suggest that the expression status of RAR-beta as a biomarker for chemoprevention/early diagnosis or the prognosis of NSCLC requires further consideration.
  • [MeSH-major] Biomarkers, Tumor / metabolism. Carcinoma, Non-Small-Cell Lung / metabolism. Lung Neoplasms / metabolism. Receptors, Retinoic Acid / metabolism. Respiratory Mucosa / pathology

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  • (PMID = 15227730.001).
  • [ISSN] 0513-5796
  • [Journal-full-title] Yonsei medical journal
  • [ISO-abbreviation] Yonsei Med. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Biomarkers, Tumor; 0 / Receptors, Retinoic Acid; 0 / retinoic acid receptor beta
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2. Zhou R, Norton JE, Zhang N, Dean DA: Electroporation-mediated transfer of plasmids to the lung results in reduced TLR9 signaling and inflammation. Gene Ther; 2007 May;14(9):775-80
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  • Electroporation can deliver DNA efficiently and safely to tissues in live animals, including the lung where it causes little inflammation or lung injury.
  • In vivo liposome-mediated gene transfer caused increases in IL-6, IL-12, tumor necrosis factor alpha and interferon gamma in mouse bronchial alveolar lavage fluid, whereas the levels of these cytokines were more than 10-fold lower by comparison following electroporation.
  • Depletion of alveolar macrophages suggested that this inflammatory response is mediated by resident pulmonary epithelial cells.

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  • (PMID = 17344904.001).
  • [ISSN] 0969-7128
  • [Journal-full-title] Gene therapy
  • [ISO-abbreviation] Gene Ther.
  • [Language] ENG
  • [Grant] United States / NHLBI NIH HHS / HL / R01 HL081148-03; United States / NHLBI NIH HHS / HL / HL71643; United States / NHLBI NIH HHS / HL / HL081148-03; United States / NHLBI NIH HHS / HL / R01 HL059956; United States / NHLBI NIH HHS / HL / HL81148; United States / NHLBI NIH HHS / HL / P01 HL071643; United States / NHLBI NIH HHS / HL / HL059956-10; United States / NHLBI NIH HHS / HL / R01 HL081148; United States / NHLBI NIH HHS / HL / HL071643-040005; United States / NHLBI NIH HHS / HL / HL59956; United States / NHLBI NIH HHS / HL / P01 HL071643-040005; United States / NHLBI NIH HHS / HL / R01 HL059956-10
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Toll-Like Receptor 9; 9007-49-2 / DNA
  • [Other-IDs] NLM/ NIHMS48103; NLM/ PMC4150868
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3. Niang A, Bonnichon A, Ba-Fall K, Dussart C, Camara P, Vaylet F, Mbaye PS, L'Her P, Sane M, Margery J: [Lung cancer in Senegal]. Med Trop (Mars); 2007 Dec;67(6):651-6
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  • The purpose of this prospective study was to analyze clinical, therapeutic, and prognostic features of lung cancer patients treated at the Principal Hospital in Dakar between 2002 and 2007.
  • Histological samples were obtained in 79.1% of cases by bronchial fibroscopy (n=33), CT-guided transthoracic needle biopsy (n=17), or from a metastatic site (n=7).
  • The histological diagnosis was squamous cell carcinoma in 23 cases, adenocarcinoma in 14, large-cell carcinoma in 17, small-cell lung cancer in 2, and bronchiolo-alveolar cancer in 1.
  • Tumor staging demonstrated grades I-II in 6 cases, grade II in 17, and grade IV in 49.
  • In the remaining cases management consisted of chemotherapy in 22 cases, radiotherapy for pain relief in 5, and surgery in 1.
  • Median survival was 7 or 3 months depending on whether or not chemotherapy was performed.
  • The much higher rate of histological diagnosis than in the sub-region is due mainly to the availability of trained personnel with access to bronchial endoscopy and CT-scan needle biopsy since September 2003.
  • Administration of cytotoxins is feasible but the cost is excessive due to the lack of universal health care coverage: two-thirds of cases were abandoned whereas chemotherapy significantly improved median survival by 4 months (p < 0.0001).
  • It is urgent to develop therapeutic standards adapted to the African socio-economic setting as well as an anti-tobacco prevention policy.
  • [MeSH-major] Carcinoma / epidemiology. Carcinoma / therapy. Lung Neoplasms / epidemiology. Lung Neoplasms / therapy
  • [MeSH-minor] Aged. Antineoplastic Agents / therapeutic use. Biopsy / methods. Female. Humans. Male. Middle Aged. Neoplasm Staging. Pneumonectomy. Prospective Studies. Senegal / epidemiology. Smoking / adverse effects. Smoking / epidemiology

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  • (PMID = 18300532.001).
  • [ISSN] 0025-682X
  • [Journal-full-title] Médecine tropicale : revue du Corps de santé colonial
  • [ISO-abbreviation] Med Trop (Mars)
  • [Language] fre
  • [Publication-type] English Abstract; Journal Article
  • [Publication-country] France
  • [Chemical-registry-number] 0 / Antineoplastic Agents
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4. Kallapur SG, Kramer BW, Moss TJ, Newnham JP, Jobe AH, Ikegami M, Bachurski CJ: Maternal glucocorticoids increase endotoxin-induced lung inflammation in preterm lambs. Am J Physiol Lung Cell Mol Physiol; 2003 Apr;284(4):L633-42
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  • Groups of ewes at 109 +/- 1 days of gestation received the following treatments: intra-amniotic (IA) saline (control), 0.5 mg/kg intramuscular Beta, 10 mg IA endotoxin (Endo), and Beta + 2 h later Endo (Beta + Endo).
  • However, compared with Endo 5 days after treatment, Beta + Endo lambs had increased alveolar neutrophils, proinflammatory cytokine mRNA expression, and serum amyloid A3 (SAA3) mRNA expression.
  • IL-1beta mRNA expression was localized to the inflammatory cells, whereas SAA3 mRNA expression was induced in the bronchial epithelium and the inflammatory cells.
  • Compared with Endo, Beta + Endo lambs had increased lung inflammation but equivalent lung volumes 15 days after treatment.
  • [MeSH-minor] Acute-Phase Reaction / immunology. Animals. Bronchoalveolar Lavage Fluid / cytology. Bronchoalveolar Lavage Fluid / immunology. Chorioamnionitis / drug therapy. Drug Synergism. Endotoxins. Female. Gene Expression / immunology. Hydrocortisone / blood. Interleukin-1 / genetics. Interleukin-6 / genetics. Interleukin-8 / genetics. Lymphocyte Count. Lymphocytes / cytology. Monocytes / cytology. Neutrophils / cytology. Pregnancy. Serum Amyloid A Protein / genetics. Sheep. Tumor Necrosis Factor-alpha / genetics

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  • (PMID = 12471018.001).
  • [ISSN] 1040-0605
  • [Journal-full-title] American journal of physiology. Lung cellular and molecular physiology
  • [ISO-abbreviation] Am. J. Physiol. Lung Cell Mol. Physiol.
  • [Language] eng
  • [Grant] United States / NICHD NIH HHS / HD / HD-12714; United States / NHLBI NIH HHS / HL / HL-65397; United States / NHLBI NIH HHS / HL / K08 HL-70711
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Endotoxins; 0 / Glucocorticoids; 0 / Interleukin-1; 0 / Interleukin-6; 0 / Interleukin-8; 0 / Serum Amyloid A Protein; 0 / Tumor Necrosis Factor-alpha; 9842X06Q6M / Betamethasone; WI4X0X7BPJ / Hydrocortisone
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5. Lee CC, Wang CN, Lai YT, Kang JJ, Liao JW, Chiang BL, Chen HC, Cheng YW: Shikonin inhibits maturation of bone marrow-derived dendritic cells and suppresses allergic airway inflammation in a murine model of asthma. Br J Pharmacol; 2010 Dec;161(7):1496-511
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  • The therapeutic potential of shikonin was evaluated in a model of allergic airway disease.
  • After intratracheal instillation of shikonin in OVA-immunized mice, OVA challenge induced lower IL-4, IL-5, IL-13, TNF-α and eotaxin release in bronchial alveolar lavage fluid, lower IL-4 and IL-5 production in lung cells and mediastinal lymph node cells and attenuated OVA-induced lung eosinophilia and airway hyperresponsiveness.
  • CONCLUSION AND IMPLICATIONS: Shikonin effectively suppressed OVA + TSLP-induced BM-DC maturation in vitro and inhibited allergic inflammation and airway hyperresponsiveness in a murine model of asthma, showing good potential as a treatment for allergic asthma.
  • Also, our model provides a novel platform for screening drugs for allergic diseases.
  • [MeSH-major] Anti-Inflammatory Agents, Non-Steroidal / pharmacology. Asthma / drug therapy. Bone Marrow Cells / drug effects. Dendritic Cells / drug effects. Naphthoquinones / pharmacology
  • [MeSH-minor] Animals. Bronchoalveolar Lavage Fluid. Cytokines / metabolism. Drugs, Chinese Herbal / metabolism. Drugs, Chinese Herbal / pharmacology. Female. Inflammation / drug therapy. Inflammation / immunology. Inflammation / pathology. Interleukin-13 / metabolism. Interleukin-4 / metabolism. Interleukin-5 / metabolism. Lung / immunology. Lung / pathology. Mice. Mice, Inbred BALB C. Ovalbumin / immunology. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 20735407.001).
  • [ISSN] 1476-5381
  • [Journal-full-title] British journal of pharmacology
  • [ISO-abbreviation] Br. J. Pharmacol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] England
  • [Chemical-registry-number] 0 / Anti-Inflammatory Agents, Non-Steroidal; 0 / Cytokines; 0 / Drugs, Chinese Herbal; 0 / Interleukin-13; 0 / Interleukin-5; 0 / Naphthoquinones; 0 / Tumor Necrosis Factor-alpha; 0 / thymic stromal lymphopoietin; 207137-56-2 / Interleukin-4; 3IK6592UBW / shikonin; 9006-59-1 / Ovalbumin
  • [Other-IDs] NLM/ PMC3010563
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6. Anabousi S, Bakowsky U, Schneider M, Huwer H, Lehr CM, Ehrhardt C: In vitro assessment of transferrin-conjugated liposomes as drug delivery systems for inhalation therapy of lung cancer. Eur J Pharm Sci; 2006 Dec;29(5):367-74
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  • [Title] In vitro assessment of transferrin-conjugated liposomes as drug delivery systems for inhalation therapy of lung cancer.
  • Here, we studied expression levels and location of TfR in different lung epithelial cell types (i.e., bronchial and alveolar epithelial cells) by flow-cytometry and confocal laser scanning microscopy (CLSM).
  • TfR was found to be expressed at a significantly higher level in bronchial epithelial cells compared with their alveolar counterparts.
  • Cells of cancerous origin (i.e., A549 cell line) showed a higher TfR expression level than healthy alveolar epithelial type II cells in primary culture.
  • Tf-conjugated liposomes appear as good candidates for an approach to deliver cytostatic drugs to sites of lung cancer by inhalation.
  • [MeSH-major] Antineoplastic Agents / administration & dosage. Drug Delivery Systems / methods. Liposomes / administration & dosage. Lung Neoplasms / drug therapy. Respiratory Therapy / methods. Transferrin / administration & dosage
  • [MeSH-minor] Cell Line, Tumor. Doxorubicin / administration & dosage. Doxorubicin / metabolism. Doxorubicin / pharmacology. Doxorubicin / toxicity. Humans. Lung / cytology. Receptors, Transferrin / metabolism

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  • (PMID = 16952451.001).
  • [ISSN] 0928-0987
  • [Journal-full-title] European journal of pharmaceutical sciences : official journal of the European Federation for Pharmaceutical Sciences
  • [ISO-abbreviation] Eur J Pharm Sci
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Netherlands
  • [Chemical-registry-number] 0 / Antineoplastic Agents; 0 / Liposomes; 0 / Receptors, Transferrin; 0 / Transferrin; 80168379AG / Doxorubicin
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7. D'Agostini F, Mastracci L, Izzotti A, Balansky R, Pennisi TM, Steele VE, De Flora S: Modulation by phenethyl isothiocyanate and budesonide of molecular and histopathologic alterations induced by environmental cigarette smoke in mice. Cancer Prev Res (Phila); 2009 Jun;2(6):546-56
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  • However, after 4 months of exposure to ECS followed by 7 months of recovery in filtered air, the lung tumor yield was rather low.
  • After weanling, the mice exposed to ECS since birth underwent a variety of alterations of molecular and cytogenetical end points, and 11 months after birth, they exhibited significant histopathologic changes, such as pulmonary anthracosis, emphysema, hemorrhagic areas, alveolar bronchiolarization, bronchial hyperplasia, and tumors, both benign and malignant.
  • [MeSH-major] Anticarcinogenic Agents / therapeutic use. Budesonide / therapeutic use. Isothiocyanates / therapeutic use. Lung Neoplasms / prevention & control. Tobacco Smoke Pollution / adverse effects
  • [MeSH-minor] Adenoma / etiology. Adenoma / prevention & control. Age Factors. Animals. Animals, Newborn. Apoptosis / drug effects. Bone Marrow Cells / drug effects. Bone Marrow Cells / pathology. Carcinoma / etiology. Carcinoma / prevention & control. DNA Adducts / analysis. Drug Screening Assays, Antitumor. Epithelial Cells / drug effects. Epithelial Cells / pathology. Female. Lung / chemistry. Lung / drug effects. Lung Diseases / drug therapy. Lung Diseases / pathology. Male. Mice. Precancerous Conditions / drug therapy. Precancerous Conditions / pathology. Pregnancy. Time Factors

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  • (PMID = 19491290.001).
  • [ISSN] 1940-6215
  • [Journal-full-title] Cancer prevention research (Philadelphia, Pa.)
  • [ISO-abbreviation] Cancer Prev Res (Phila)
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CN / N01-CN53301
  • [Publication-type] Journal Article; Research Support, N.I.H., Extramural
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Anticarcinogenic Agents; 0 / DNA Adducts; 0 / Isothiocyanates; 0 / Tobacco Smoke Pollution; 51333-22-3 / Budesonide; 6U7TFK75KV / phenethyl isothiocyanate
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8. Melamed J, Kernizan S, Walden PD: Expression of B-cell translocation gene 2 protein in normal human tissues. Tissue Cell; 2002 Feb;34(1):28-32
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  • [Title] Expression of B-cell translocation gene 2 protein in normal human tissues.
  • The objective of the present study was to provide further insight into the biological function of BTG2(TIS21/PC3) by determining the expression levels and cellular localization of BTG2(TIS21/PC3) in a spectrum of normal human tissues and to determine the proliferative indices (based on Ki-67 staining) and apoptotic indices (based on TUNEL assay) in those cell populations where BTG2(TIS21/PC3) was differentially expressed.
  • Highest levels of BTG2(TIS21/PC3) expression were seen in kidney proximal tubules, lung alveolar bronchial epithelium and in the basal cell layer of prostate acini.
  • BTG2(TIS21/PC3) was expressed at significantly different levels within the different epithelial populations of the kidney (proximal vs distal tubules) and prostate (acinar basal cells vs lumenal cells).
  • [MeSH-major] Apoptosis / genetics. Cell Cycle Proteins / biosynthesis. Cell Division / genetics. Genes, Tumor Suppressor. Immediate-Early Proteins / biosynthesis
  • [MeSH-minor] Humans. Immunohistochemistry. Organ Specificity / genetics. Tumor Suppressor Proteins

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  • (PMID = 11989967.001).
  • [ISSN] 0040-8166
  • [Journal-full-title] Tissue & cell
  • [ISO-abbreviation] Tissue Cell
  • [Language] eng
  • [Grant] United States / NCI NIH HHS / CA / R01 CA 84441; United States / NCI NIH HHS / CA / U01 CA 86743
  • [Publication-type] Journal Article; Research Support, U.S. Gov't, P.H.S.
  • [Publication-country] Scotland
  • [Chemical-registry-number] 0 / Cell Cycle Proteins; 0 / Immediate-Early Proteins; 0 / Tumor Suppressor Proteins; 141490-22-4 / BTG2 protein, human
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9. Xia XM, Wang FY, Wang ZK, Wan HJ, Xu WA, Lu H: Emodin enhances alveolar epithelial barrier function in rats with experimental acute pancreatitis. World J Gastroenterol; 2010 Jun 28;16(24):2994-3001
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  • [Title] Emodin enhances alveolar epithelial barrier function in rats with experimental acute pancreatitis.
  • AIM: To investigate the effect of emodin on expression of claudin-4, claudin-5 and occludin, as well as the alveolar epithelial barrier in rats with pancreatitis induced by sodium taurocholate.
  • Rats from sham operation group and acute pancreatitis group were injected with normal saline (an equivalent volume as emodin) at the same time point.
  • Samples of lung and serum were obtained 6 h after drug administration.
  • Pulmonary edema was estimated by measuring water content in lung tissue samples.
  • Tumor necrosis factor-alpha (TNF-alpha) and interleukin-6 (IL-6) level were measured by enzyme-linked immunospecific assay.
  • Alveolar epithelial barrier was assessed by pulmonary dye extravasation.
  • Expression of claudin-4, claudin-5 and occludin in lung tissue samples was examined by immunohistology, quantitative real-time reverse transcription polymerase chain reaction and Western blotting analysis, respectively.
  • RESULTS: Pancreatitis-associated lung injury was characterized by pulmonary edema, leukocyte infiltration, alveolar collapse, and elevated serum amylase level.
  • The pulmonary damage, pulmonary pathological scores, serum amylase and MPO activity, TNF-alpha and IL-6 levels, and wet/dry ratio were decreased in rats after treatment with emodin.
  • Immunostaining of claudin-4, claudin-5 and occludin was detected in lung tissue samples from rats in sham operation group, which was distributed in alveolar epithelium, vascular endothelium, and bronchial epithelium, respectively.
  • The mRNA and protein expression levels of claudin-4, claudin-5 and occludin in lung tissue samples were markedly decreased, the expression level of claudin-4, claudin-5 and occluding was increased, and the pulmonary dye extravasation was reduced in lung tissue samples from rats with acute pancreatitis after treatment with emodin.
  • CONCLUSION: Emodin attenuates pulmonary edema and inflammation, enhances alveolar epithelial barrier function, and promotes expression of claudin-4, claudin-5 and occludin in lung tissue samples from rats with acute pancreatitis.
  • [MeSH-major] Blood-Air Barrier / drug effects. Emodin. Pancreatitis / drug therapy. Pancreatitis / pathology. Pulmonary Alveoli
  • [MeSH-minor] Animals. Claudin-4. Claudin-5. Lung / anatomy & histology. Lung / drug effects. Lung / metabolism. Lung / pathology. Male. Membrane Proteins / genetics. Membrane Proteins / metabolism. Occludin. Protein Kinase Inhibitors / pharmacology. Protein Kinase Inhibitors / therapeutic use. Pulmonary Edema / drug therapy. Pulmonary Edema / etiology. Pulmonary Edema / physiopathology. Random Allocation. Rats. Rats, Sprague-Dawley. Taurocholic Acid / pharmacology

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  • (PMID = 20572302.001).
  • [ISSN] 2219-2840
  • [Journal-full-title] World journal of gastroenterology
  • [ISO-abbreviation] World J. Gastroenterol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] China
  • [Chemical-registry-number] 0 / Claudin-4; 0 / Claudin-5; 0 / Cldn5 protein, rat; 0 / Membrane Proteins; 0 / Occludin; 0 / Ocln protein, rat; 0 / Protein Kinase Inhibitors; 5E090O0G3Z / Taurocholic Acid; KA46RNI6HN / Emodin
  • [Other-IDs] NLM/ PMC2890939
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10. Chung KF: Cytokines as targets in chronic obstructive pulmonary disease. Curr Drug Targets; 2006 Jun;7(6):675-81
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  • Increased interleukin [IL]-6, IL-1beta, tumor necrosis factor-alpha [TNF-alpha], GRO-alpha, MCP-1 and IL-8 levels are measured in sputum, with further increases during exacerbations.
  • TNFalpha and IL-1beta stimulate macrophages to produce matrix metalloproteinase-9 [MMP-9], and bronchial epithelial cells to produce extracellular matrix glycoproteins.
  • Anti-cytokine therapy could be in the form of soluble receptors or by neutralising antibodies, small compounds blocking cytokine receptors or incomplete and non-activating cytokines, inhibitors of protein activation and inhibitors of signal transduction and transcription such as via inhibition of mitogen-activated protein kinases [MAPK] and of transcription factor, nuclear factor kappaB.
  • Anti-IL-8 therapy has been tried with little effect on COPD, and current trials are on-going with TNF-alpha inhibitors.
  • Other treatments such as phosphodiesterase 4 inhibitors have anti-cytokine effects that may underlie their beneficial effects in COPD.
  • [MeSH-major] Cytokines / immunology. Pulmonary Disease, Chronic Obstructive / drug therapy
  • [MeSH-minor] Adrenal Cortex Hormones / administration & dosage. Adrenal Cortex Hormones / pharmacology. Adrenal Cortex Hormones / therapeutic use. Animals. Humans. Macrophages, Alveolar / drug effects. Macrophages, Alveolar / immunology. Phosphodiesterase Inhibitors / administration & dosage. Phosphodiesterase Inhibitors / pharmacology. Phosphodiesterase Inhibitors / therapeutic use. Receptors, Cytokine / antagonists & inhibitors. Respiratory Mucosa / drug effects. Respiratory Mucosa / immunology


11. Hukkanen J, Väisänen T, Lassila A, Piipari R, Anttila S, Pelkonen O, Raunio H, Hakkola J: Regulation of CYP3A5 by glucocorticoids and cigarette smoke in human lung-derived cells. J Pharmacol Exp Ther; 2003 Feb;304(2):745-52
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  • About 4-fold induction was detected by nanomolar concentrations of dexamethasone and also by budenoside and beclomethasone dipropionate, glucocorticoids used for the inhalation treatment of bronchial asthma, whereas the CYP3A4 inducers mifepristone (RU486), rifampicin, clotrimazole, and nifedipine were without effect.
  • In transient transfection assays to A549 cells, CYP3A5 5' regulatory region was activated by the dexamethasone treatment.
  • The CYP3A5 expression was measured in alveolar macrophages from patients with respiratory diseases.
  • The CYP3A5 expression level was decreased by smoking, but glucocorticoid therapy had no statistically significant effect.
  • [MeSH-major] Cytochrome P-450 Enzyme System / biosynthesis. Glucocorticoids / pharmacology. Lung / cytology. Lung / drug effects. Smoking / metabolism
  • [MeSH-minor] Analysis of Variance. Animals. COS Cells. Cercopithecus aethiops. Cytochrome P-450 CYP3A. Humans. Macrophages, Alveolar / cytology. Macrophages, Alveolar / drug effects. Macrophages, Alveolar / enzymology. RNA, Messenger / biosynthesis. Respiratory Mucosa / cytology. Respiratory Mucosa / drug effects. Respiratory Mucosa / enzymology. Tumor Cells, Cultured

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  • (PMID = 12538830.001).
  • [ISSN] 0022-3565
  • [Journal-full-title] The Journal of pharmacology and experimental therapeutics
  • [ISO-abbreviation] J. Pharmacol. Exp. Ther.
  • [Language] eng
  • [Publication-type] Comparative Study; Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Glucocorticoids; 0 / RNA, Messenger; 9035-51-2 / Cytochrome P-450 Enzyme System; EC 1.14.13.67 / CYP3A4 protein, human; EC 1.14.14.1 / CYP3A protein, human; EC 1.14.14.1 / CYP3A5 protein, human; EC 1.14.14.1 / Cytochrome P-450 CYP3A
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12. Wu Y, Singer M, Thouron F, Alaoui-El-Azher M, Touqui L: Effect of surfactant on pulmonary expression of type IIA PLA(2) in an animal model of acute lung injury. Am J Physiol Lung Cell Mol Physiol; 2002 Apr;282(4):L743-50
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  • [Title] Effect of surfactant on pulmonary expression of type IIA PLA(2) in an animal model of acute lung injury.
  • We previously showed that the seminatural surfactant Curosurf inhibits the in vitro synthesis of secretory type IIA phospholipase A(2) (sPLA(2)-IIA) in alveolar macrophages (AM).
  • Curosurf instillation 30 min or 8 h after LPS reversed the increase in tumor necrosis factor-alpha expression, polymorphonuclear cell extravasation, and protein concentration in bronchoalveolar lavage fluids.
  • Curosurf also decreased the bronchial reactivity induced by LPS.
  • [MeSH-major] Biological Products. Lung / enzymology. Phospholipases A / metabolism. Phospholipids. Pulmonary Surfactants / pharmacology. Respiratory Distress Syndrome, Adult / drug therapy. Respiratory Distress Syndrome, Adult / metabolism
  • [MeSH-minor] Acute Disease. Animals. Bronchial Hyperreactivity / chemically induced. Bronchial Hyperreactivity / drug therapy. Bronchial Hyperreactivity / metabolism. Bronchoalveolar Lavage Fluid / cytology. Cell Count. Disease Models, Animal. Gene Expression / drug effects. Group II Phospholipases A2. Guinea Pigs. Lipopolysaccharides / pharmacology. Macrophages, Alveolar / metabolism. Male. Pneumonia / chemically induced. Pneumonia / drug therapy. Pneumonia / metabolism. RNA, Messenger / analysis. Tumor Necrosis Factor-alpha / genetics. Tumor Necrosis Factor-alpha / metabolism

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  • (PMID = 11880300.001).
  • [ISSN] 1040-0605
  • [Journal-full-title] American journal of physiology. Lung cellular and molecular physiology
  • [ISO-abbreviation] Am. J. Physiol. Lung Cell Mol. Physiol.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] United States
  • [Chemical-registry-number] 0 / Biological Products; 0 / Lipopolysaccharides; 0 / Phospholipids; 0 / Pulmonary Surfactants; 0 / RNA, Messenger; 0 / Tumor Necrosis Factor-alpha; EC 3.1.1.- / Phospholipases A; EC 3.1.1.4 / Group II Phospholipases A2; KE3U2023NP / poractant alfa
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13. Chorianopoulos D, Samitas K, Vittorakis S, Kiriazi V, Rondoyianni D, Tsaousis G, Skoutelis A: Extranodal natural killer/T-cell lymphoma, nasal-type. Skinmed; 2010 Jan-Feb;8(1):56-8
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  • [Title] Extranodal natural killer/T-cell lymphoma, nasal-type.
  • Computed tomograph (CT) of the chest showed multiple alveolar opacities bilaterally (Figure 2).
  • Results of bronchial biopsy, cytology of bronchoalveolar lavage, washing, brushing, and sputum following bronchoscopy were negative.
  • Immunohistochemical stains showed that the tumor cell were positive for CD56 and CD3 (cytoplasmic positivity) and expressed the cytotoxic proteins T-cell intracellular antigen and granzyme B (Figure 3) They lacked TdT, CD34, CD7, CD8, TCL-1, and CD123.
  • The morphology and the immunophenotype were consistent with natural killer/T-cell lymphoma, nasal-type.
  • Nasal involvement must be first excluded to proceed to the diagnosis of nasal-type natural killer-cell lymphoma.
  • Thus, the authors were led to the diagnosis of extranodal extranasal natural killer/T-cell lymphoma, nasal-type, CD56-positive, Ep stein-Barr virus-negative, TCR-negative.
  • The patient received combination chemotherapy and completed 4 cycles of cyclophosphamide, doxorubicin vincristine, and prednisone every 14 days for 2 months.
  • Skin lesions improved, and there was no fever soon after the initiation of therapy.
  • The patient had receive systemic salvage chemotherapy and intrathecal infusions of methotrexate.
  • Although the lung lesions had diminished at that time, the patient develope paraplegia, his clinical course rapidly deteriorated, and he eventually died.

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  • (PMID = 20839428.001).
  • [ISSN] 1540-9740
  • [Journal-full-title] Skinmed
  • [ISO-abbreviation] Skinmed
  • [Language] eng
  • [Publication-type] Case Reports; Journal Article
  • [Publication-country] United States
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