Only in Titles

           Search results for: cDNA _ Emphysema Lung   

paperclip

#29419339   // Save this To Up

Emphysema induced by elastase alters the mRNA relative levels from DNA repair genes in acute lung injury in response to sepsis induced by lipopolysaccharide administration in Wistar rats.

Purpose/Aim of the study: Patients suffering from chronic obstructive pulmonary disease (COPD) in association with acute respiratory distress syndrome (ARDS) present oxidative stress in lung cells, with production of free radicals and DNA lesions in pulmonary and adjacent cells. Once the DNA molecule is damaged, a set of enzymatic mechanisms are trigged to preserve genetic code integrity and cellular homeostasis. These enzymatic mechanisms include the base and the nucleotide excision repair pathways, as well as telomere regulation. Thus, the aim of this work was to evaluate the mRNA levels from APEX1, ERCC2, TP53, and TRF2 genes in lung tissue from Wistar rats affected by acute lung injury in response to sepsis and emphysema.

1980 related Products with: Emphysema induced by elastase alters the mRNA relative levels from DNA repair genes in acute lung injury in response to sepsis induced by lipopolysaccharide administration in Wistar rats.

OxiSelect™ Cellular UV- Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Human Epstein-Barr Virus Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Jurkat Cell Extract (Indu Mouse Epstein-Barr Virus TGF beta induced factor 2

Related Pathways

paperclip

#29111769   // Save this To Up

XPC Deficiency Alters Cigarette Smoke DNA Damage Cell Fate and Accelerates Emphysema Development.

Cigarette smoke (CS) exposure is a major risk factor for the development of emphysema, a common disease characterized by loss of cells comprising the lung parenchyma. The mechanisms of cell injury leading to emphysema are not completely understood but are thought to involve persistent cytotoxic or mutagenic DNA damage induced by CS. Using complementary cell culture and mouse models of CS exposure, we investigated the role of the DNA repair protein xeroderma pigmentosum group C (XPC) on CS-induced DNA damage repair and emphysema. Expression of XPC was decreased in mouse lungs following chronic CS exposure and XPC knock-down in cultured human lung epithelial cells decreased their survival following CS exposure due to activation of the intrinsic apoptosis pathway. Similarly, cell autophagy and apoptosis were increased in XPC-deficient mouse lungs and were further increased by CS exposure. XPC deficiency was associated with structural and functional changes characteristic of emphysema, which were worsened by age similar to levels observed with chronic CS exposure. Taken together, these findings suggest that repair of DNA damage by XPC plays an important and previously unrecognized role in the maintenance of alveolar structures. These findings support that loss of XPC, possibly due to chronic CS exposure, promotes emphysema development and further supports a link between DNA damage, impaired DNA repair and development of emphysema.

1889 related Products with: XPC Deficiency Alters Cigarette Smoke DNA Damage Cell Fate and Accelerates Emphysema Development.

OxiSelect™ Cellular UV- DNA (cytosine 5) methyltr AccuPrep Genomic DNA Extr DiscoveryPak™ Stem Cell DiscoveryPak™ Stem Cell DiscoveryPak™ Stem Cell DiscoveryPak™ Stem Cell DiscoveryPak™ Stem Cell DiscoveryPak™ Stem Cell DiscoveryPak™ Stem Cell FitAmp Blood and Cultured  FitAmp Blood and Cultur

Related Pathways

paperclip

#26620975   // Save this To Up

The rs361525 polymorphism does not increase production of tumor necrosis factor alpha by monocytes from alpha-1 antitrypsin deficient subjects with chronic obstructive pulmonary disease - a pilot study.

Polymorphisms in the TNF-A gene have been associated with chronic obstructive pulmonary disease (COPD) in some case-control studies. Previous work has shown that COPD/chronic bronchitis subjects with alpha-1 antitrypsin deficiency with the rs361525 TNF-α single nucleotide polymorphism have 100 times more TNF-in spontaneous sputum than disease matched controls. Our objective was to determine if the presence of this polymorphism increased TNF-α production by blood monocytes from COPD subjects.

2142 related Products with: The rs361525 polymorphism does not increase production of tumor necrosis factor alpha by monocytes from alpha-1 antitrypsin deficient subjects with chronic obstructive pulmonary disease - a pilot study.

Human Tumor Necrosis Fact ELISA Kit for Tumor Necr TNFRSF1B - Goat polyclona Mouse Tumor Necrosis Fact Rat Tumor Necrosis Factor ELISA Kit for Tumor Necro Mouse Tumor Necrosis Fact Human Tumor Necrosis Fact Tumor necrosis factor (TN RABBIT ANTI HUMAN SDF-1 A RANK Ligand Soluble, Huma Contact Factors: Human al

Related Pathways

paperclip

#25440386   // Save this To Up

Therapeutic potential of Panax ginseng and ginsenosides in the treatment of chronic obstructive pulmonary disease.

Chronic obstructive pulmonary disease (COPD) is a major global health burden and will become the third largest cause of death in the world by 2030. It is currently believed that an exaggerated inflammatory response to inhaled irritants, in particular cigarette smoke, cause progressive airflow limitation. This inflammation, where macrophages, neutrophils and lymphocytes are prominent, leads to oxidative stress, emphysema, airways fibrosis and mucus hypersecretion. COPD responds poorly to current anti-inflammatory treatments including corticosteroids, which produce little or no benefit. Panax ginseng has a long history of use in Chinese medicine for respiratory conditions, including asthma and COPD.

2277 related Products with: Therapeutic potential of Panax ginseng and ginsenosides in the treatment of chronic obstructive pulmonary disease.

Anti 3 DG imidazolone Mon FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu Multiple organ tumor tiss Beta Amyloid (42) ELISA K Beta Amyloid (1 40) ELISA Beta Amyloid (40) ELISA K Beta Amyloid (1 40) ELISA

Related Pathways

paperclip

#21115650   // Save this To Up

Admixture mapping of lung cancer in 1812 African-Americans.

Lung cancer continues to be the leading cause of cancer death in the USA and the best example of a cancer with undisputed evidence of environmental risk. However, a genetic contribution to lung cancer has also been demonstrated by studies of familial aggregation, family-based linkage, candidate gene studies and most recently genome-wide association studies (GWAS). The African-American population has been underrepresented in these genetic studies and has patterns of cigarette use and linkage disequilibrium that differ from patterns in other populations. Therefore, studies in African-Americans can provide complementary data to localize lung cancer susceptibility genes and explore smoking dependence-related genes. We used admixture mapping to further characterize genetic risk of lung cancer in a series of 837 African-American lung cancer cases and 975 African-American controls genotyped at 1344 ancestry informative single-nucleotide polymorphisms. Both case-only and case-control analyses were conducted using ADMIXMAP adjusted for age, sex, pack-years of smoking, family history of lung cancer, history of emphysema and study site. In case-only analyses, excess European ancestry was observed over a wide region on chromosome 1 with the largest excess seen at rs6587361 for non-small-cell lung cancer (NSCLC) (Z-score = -4.33; P = 1.5 × 10⁻⁵) and for women with NSCLC (Z-score = -4.82; P = 1.4 × 10⁻⁶). Excess African ancestry was also observed on chromosome 3q with a peak Z-score of 3.33 (P = 0.0009) at rs181696 among ever smokers with NSCLC. These results add to the findings from the GWAS in Caucasian populations and suggest novel regions of interest.

2529 related Products with: Admixture mapping of lung cancer in 1812 African-Americans.

Lung cancer tissue array, Lung cancer tissue array Colon cancer and lung can Lung non small cell cance Lung cancer tissue array, Lung cancer survey tissue Lung cancer survey tissue Lung cancer tissue array Lung cancer tissue array Lung cancer tissue array Lung cancer tissue array Lung cancer tissue array

Related Pathways

paperclip

#20372105   // Save this To Up

Expression of human alpha1-antitrypsin in mice and dogs following AAV6 vector-mediated gene transfer to the lungs.

We evaluated the potential of lung-directed gene therapy for alpha1-antitrypsin (AAT) deficiency using an adeno-associated virus type 6 (AAV6) vector containing a human AAT (hAAT) complementary DNA (cDNA) delivered to the lungs of mice and dogs. The results in normal and immune-deficient mice showed that hAAT concentrations were much higher in lung fluid than in plasma, and therapeutic levels were obtained even in normal mice. However, in normal mice an immune response against the vector and/or transgene limited long-term gene expression. An AAV6 vector expressing a marker protein verified that AAV6 vectors efficiently transduced lung cells in dogs. Delivery of AAV6-hAAT resulted in low levels of hAAT in dog serum but therapeutic levels in the lung that persisted for at least 58 days to 4 months in three immunosuppressed dogs. Expression in the serum was not detectable after 45 days in one nonimmune suppressed dog. A lymphoproliferative response to AAV capsid but not to hAAT was detected even after immunosuppression. These results in mice and dogs show the feasibility of expression of therapeutic levels of AAT in the lungs after AAV vector delivery, and advocate for approaches to prevent cellular immune responses to AAV capsid proteins for persistence of gene expression in humans.

1268 related Products with: Expression of human alpha1-antitrypsin in mice and dogs following AAV6 vector-mediated gene transfer to the lungs.

DNA (cytosine 5) methyltr Human Epstein-Barr Virus Recombinant Human Interfe Goat Anti-Human Catenin a Goat Anti-Human TOM1L1 SR FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu FDA Standard Frozen Tissu pYLEX1 - Expression Vect pCdgCAT Mammalian CAT Exp pCAMBIA0105.1R Vector, (G

Related Pathways

paperclip

#20443867   // Save this To Up

Emphysema mediated by lung overexpression of ADAM10.

Cigarette smoking is the major risk factor for emphysema, a disorder of the lung parenchyma characterized by destruction of the alveolar walls. Current concepts of the pathogenesis of emphysema hold that the destruction of the lung parenchyma results, in part, from a local imbalance of proteases and antiproteases. Based on the knowledge that human alveolar macrophages express ADAM 10, a protease capable of destroying basement membrane collagen but not previously implicated in emphysema, we used adenovirus-mediated lung expression of ADAM 10 in a mouse model to assess whether an increased burden of ADAM 10 was capable of inducing emphysema. To assess this, the human ADAM 10 cDNA under control of a constitutive promoter was inserted into an adenovirus gene transfer vector (AdhADAMlO), and the vector (10(11) particle units) administered to the respiratory tract of wild type C57BI/6 mice. Lung levels of ADAM 10 mRNA and protein were upregulated following AdhADAMlO administration. After 8 weeks, quantitative morphometry of the lung parenchyma demonstrated that AdhADAMlO administration induced emphysema (mean linear intercept of 60.6 + 1.3 microm compared with 55.6 + 0.8 in mice treated with a control vector, p < 0.003). These results suggest a role of ADAM 10 in the pathogenesis of emphysema, adding to the list of proteases expressed in the lung that are capable of contributing to the development of lung destruction.

1174 related Products with: Emphysema mediated by lung overexpression of ADAM10.

Mouse Anti-Human Lung Ag. Recombinant Human ADAM10 Recombinant Human ADAM10 Recombinant Human ADAM10 Primary antibody ADAM10 Anti RAGE (Receptor for A ADAM10 Antibody Lung disease spectrum tis Lung cancer tissue array, Lung carcinoma (multi tis Non small cell lung carci Non small cell lung carci

Related Pathways

paperclip

#18323534   // Save this To Up

Sustained expression of alpha1-antitrypsin after transplantation of manipulated hematopoietic stem cells.

Inherited mutations in the human alpha(1)-antitrypsin (AAT) gene lead to deficient circulating levels of AAT protein and a predisposition to developing emphysema. Gene therapy for individuals deficient in AAT is an attractive goal, because transfer of a normal AAT gene into any cell type able to secrete AAT should reverse deficient AAT levels and attenuate progression of lung disease. Here we present an approach for AAT gene transfer based on the transplantation of lentivirally transduced hematopoietic stem cells (HSCs). We develop a novel dual-promoter lentiviral system to transfer normal human AAT cDNA as well as a fluorescent tracking "reporter gene" into murine HSCs. After transplantation of 3,000 transduced HSCs into irradiated mouse recipients, we demonstrate simultaneous and sustained systemic expression of both genes in vivo for at least 31 weeks. The stem cells transduced with this protocol maintain multipotency, self-renewal potential, and the ability to reconstitute the hematopoietic systems of both primary and secondary recipients. This lentiviral-based system may be useful for investigations requiring the systemic secretion of anti-proteases or cytokines relevant to the pathogenesis of a variety of lung diseases.

1714 related Products with: Sustained expression of alpha1-antitrypsin after transplantation of manipulated hematopoietic stem cells.

Alpha1-Antitrypsin Alpha1-Antitrypsin Alpha1-Antitrypsin Macrophage Colony Stimula Macrophage Colony Stimula anti CD34 Hematopoietic p anti CD38 Hematopoietic p Stemez hN2 Human Neuron D pDC57 Mammalian Luciferas pDC99 Mammalian Luciferas Ofloxacin CAS Number [824 129 Mouse Embryonic Stem

Related Pathways

paperclip

#17400729   // Save this To Up

Pulmonary inflammation and emphysema: role of the cytokines IL-18 and IL-13.

Chronic obstructive pulmonary disease (COPD) is believed to be an inflammatory cytokine-driven disease, but a causal basis that can be associated with a specific cytokine has not been directly demonstrated. We have previously reported that proinflammatory cytokine IL-18 expression is important in the pathogenesis of pulmonary inflammation and lung injury in mice. Our results demonstrate that IL-18 overproduction in the lungs can induce lung diseases, such as pulmonary inflammation, lung fibrosis, and COPD.

2283 related Products with: Pulmonary inflammation and emphysema: role of the cytokines IL-18 and IL-13.

IL (Mouse) Quantitative A IL (Mouse) Quantitative A Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 AZD-3514 Mechanisms: Andr 17β-Acetoxy-2α-bromo-5 (5α,16β)-N-Acetyl-16-[2 (5α,16β)-N-Acetyl-16-ac 5α-N-Acetyl-2'H-androst-

Related Pathways

paperclip

#16504044   // Save this To Up

Lung fibroblasts from patients with emphysema show markers of senescence in vitro.

The loss of alveolar walls is a hallmark of emphysema. As fibroblasts play an important role in the maintenance of alveolar structure, a change in fibroblast phenotype could be involved in the pathogenesis of this disease. In a previous study we found a reduced in vitro proliferation rate and number of population doublings of parenchymal lung fibroblasts from patients with emphysema and we hypothesized that these findings could be related to a premature cellular aging of these cells. In this study, we therefore compared cellular senescence markers and expression of respective genes between lung fibroblasts from patients with emphysema and control patients without COPD.

2783 related Products with: Lung fibroblasts from patients with emphysema show markers of senescence in vitro.

Anti 3 DG imidazolone Mon Cultrex In Vitro Angiogen Lung disease spectrum tis Lung cancer tissue array, Lung carcinoma and normal Lung carcinoma and normal Lung cancer tissue array Lung squamous cell carcin Lung adenocarcinoma and n Lung adenocarcinoma tissu Breast cancer tissue arra Breast disease spectrum t

Related Pathways