Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0001511 (Adhesion)
 5,955 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The biochemical holding strength and histological characteristics of a laparoscopic stapled gastropexy (LG) adhesion were compared with that of an incisional gastropexy (IG) adhesion. An LG was performed in 14 dogs and an IG was performed in six dogs. During the LG procedure, the abdomen was insufflated with carbon dioxide and three cannulae were placed in the caudal aspect of the right side of the abdomen. A 35 mm laparoscopic stapler was used to staple the gastric antrum to the adjacent right lateral abdominal wall. The IG procedure was performed through ventral midline celiotomy. A 35 mm IG was made by apposing the gastric antrum to the adjacent right lateral abdominal wall with two continuous rows of suture. Half of each group of dogs was euthanatized at 7 and 30 days after surgery. The mean tensile load to failure at 7 days was 44.86 +/- 18.54 N for the LG group and 85.33 +/- 23.59 N for the IG group (P < .05). At 30 days the values were 72.39 +/- 18.01 N for the LG group and 71.17 +/-12.11 N for the IG group (P = .41). The gastropexy adhesions in the 7-day postoperative group contained variable amounts of fibrin, hemorrhage, mononuclear cell inflammation, loose fibrovascular tissue, and mature collagenous connective tissue. Adhesions in the 7-day postoperative group were divided subjectively into three histological subgroups based on the relative amounts of mature connective tissue within the adhesion. The LG and IG adhesions were randomly distributed among these subgroups (P = 1.0). Adhesions in the 30-day postoperative group contained well-organized fibrous connective tissue. No difference in the amount of connective tissue could be detected histologically in the LG or IG adhesions. Complications with the LG procedure included stomach perforation (2 cases), splenic puncture (2 cases), and subcutaneous emphysema (4 cases).
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PMID:Biomechanical and histological evaluation of a laparoscopic stapled gastropexy technique in dogs. 892 90

Chronic inhalation of coal dust can cause several lung disorders, including simple coal workers pneumoconiosis (CWP), progressive massive fibrosis (PMF), chronic bronchitis, lung function loss, and emphysema. This review focuses on the cellular actions and interactions of key inflammatory cells and target cells in coal dust toxicity and related lung disorders, i.e. macrophages and neutrophils, epithelial cells, and fibroblasts. Factors released from or affecting these cells are outlined in separate sections, i.e. (1) reactive oxygen species (ROS) and related antioxidant protection mechanisms, and (2) cytokines, growth factors and related proteins. Furthermore, (3) components of the extracellular matrix (ECM), including the modifying role of ROS, cytokines, proteases and antiproteases are discussed in relation to tissue damage and remodelling in the respiratory tract. It is recognised that inhaled coal dust particles are important non-cellular and cellular sources of ROS in the lung, and may be significantly involved in the damage of lung target cells as well as important macromolecules including alpha-1-antitrypsin and DNA. In vitro and in vivo studies with coal dusts showed the up-regulation of important leukocyte recruiting factors, e.g. Leukotriene-B4 (LTB4), Platelet Derived Growth Factor (PDGF), Monocyte Chemotactic Protein-1 (MCP-1), and Tumor Necrosis Factor-alpha (TNF alpha), as well as the neutrophil adhesion factor Intercellular Adhesion Molecule-1 (ICAM-1). Coal dust particles are also known to stimulate the (macrophage) production of various factors with potential capacity to modulate lung cells and/or extracellular matrix, including O2-., H2O2, and NO, fibroblast chemoattractants (e.g. Transforming Growth Factor-beta (TGF beta), PDGF, and fibronectin) and a number of factors that have been shown to stimulate and/or inhibit fibroblast growth or collagen production such as (TNF alpha, TGF beta, PDGF, Insulin Like Growth Factor, and Prostaglandin-E2). Further studies are needed to clarify the in vivo kinetics and relative impact of these factors.
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PMID:Mechanisms and mediators in coal dust induced toxicity: a review. 1002 91

Pulmonary emphysema in chronic obstructive pulmonary disease (COPD) is characterized by the destruction of the alveolar walls leading to permanent enlargement of distal respiratory air spaces. A major causal factor is cigarette smoking, which produces conditions of chronic oxidative stress within the lungs. At a cellular level, increased macrophage accumulation and retention within the alveolar interstitial spaces is pivotal to the development of emphysema. To date it has been unclear as to the underlying mechanisms relating chronic oxidative stress to macrophage accumulation and retention. Our study was initiated to ascertain the role of modification of extracellular matrix proteins with cigarette smoke and products of lipid peroxidation on macrophage adhesion and activation. Increased numbers of macrophages were seen adhering to cigarette smoke-modified collagen IV as compared to unmodified collagen, where little or no adherent macrophages were observed. Similar observations were made when collagen was modified with either acrolein or 4-hydroxy-2-nonenal. Adhesion could be blocked with either fucoidan or a monoclonal antibody against the Type A macrophage scavenger receptor. Also, modified collagen triggered both oxidative burst and MCP-1 release in macrophages. These results, therefore, highlight a potential mechanism by which oxidative stress through the production of reactive carbonyls promotes macrophage accumulation, retention, and activation, independently of other proinflammatory stimuli. The implications of this for the development of emphysema in COPD are discussed.
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PMID:Cigarette smoke triggers macrophage adhesion and activation: role of lipid peroxidation products and scavenger receptor. 1458 34