Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objective of this pilot study was to evaluate the safety and success of early tracheal extubation (ETE) as compared to delayed tracheal extubation (DTE) in single-lung transplantation (SLT) for chronic obstructive pulmonary disease (COPD). This retrospective observational study was undertaken at a university hospital. Fifty-seven adult patients who underwent SLT for COPD (1998-2003) were enrolled. The study cohort was divided into an ETE subgroup (tracheal extubation in the operating room) or a DTE subgroup (tracheal extubation in the intensive care unit). There were no significant differences in perioperative outcomes between subgroups (in-hospital mortality; length of stay; prolonged mechanical ventilation; primary graft dysfunction; pneumonia; atrial fibrillation; renal dysfunction; and, sepsis). The anesthetic technique associated with ETE in SLT for COPD was characterized by limited systemic anesthetics and perioperative thoracic epidural analgesia. Appropriate ETE in SLT for COPD is not only safe but also results in equivalent perioperative outcome when compared to the traditional technique of DTE. Future studies should be powered to examine whether ETE reduces native lung complications such as hyperinflation, pneumonia and pneumothorax.
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PMID:Early tracheal extubation in adults undergoing single-lung transplantation for chronic obstructive pulmonary disease: pilot evaluation of perioperative outcome. 1862 42

Chronic inflammation and acute exacerbations are pathophysiological features of chronic obstructive pulmonary disease (COPD). An impaired immune response to bacterial pathogens can contribute to both of them. Nucleotide oligomerization domain 2 (NOD2) is an intracellular receptor of innate immunity for muramyldipeptide (MDP). Mutations of the NOD2 gene followed by decreased recognition of MDP are associated with chronic intestinal inflammation and pulmonary complications of patients with allogenic stem cell transplant and sepsis. Our study provides evidence that NOD2, toll-like receptor 4 (TLR4) and the adapter protein receptor-interacting protein 2 (RIP2) are induced by tumor-necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma) in the bronchial epithelial cell line BEAS-2B. We also demonstrate that lipopolysaccharide (LPS) can further increase NOD2 transcription in a TNF-alpha and IFN-gamma-induced activation state. In addition, we show that, while MDP fails to enhance CXCL-8 release from otherwise unstimulated BEAS-2B cells, a 12 h prestimulation period with TNF-alpha and IFN-gamma primes the cells for an additional increase of CXCL-8 secretion via induction of NOD2 and RIP2. LPS itself significantly augments CXCL-8 production and co-administration of MDP further increases cytokine secretion. Finally, overexpression of an SNP13 mutant decreased MDP-induced chemokine production in BEAS-2B cells compared with NOD2 wild type overexpression. Taken together, our work indicates that MDP and NOD2 play an important role for CXCL-8 release of BEAS-2B cells following LPS-challenge via synergistic interactions between MDP and LPS.
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PMID:Muramyldipeptide modulates CXCL-8 release of BEAS-2B cells via NOD2. 1864 46

Sphingolipids such as sphingosine-1-phosphate (S1P), ceramide, or sphingomyelin are essential constituents of plasma membranes and regulate many (patho)physiological cellular responses inducing apoptosis and cell survival, vascular permeability, mast cell activation, and airway smooth muscle functions. The complexity of sphingolipid biology is generated by a great variety of compounds, diverse receptors, and often antagonistic functions of different sphingolipids. For instance, apoptosis is promoted by ceramide and prevented by S1P, and pulmonary vascular permeability is increased by S1P2/3 receptors and by ceramide, whereas S1P1 receptors stabilize barrier integrity. Several enzymes of the sphingolipid metabolism respond to external stimuli such as sphingomyelinase isoenzymes that are activated by many stress stimuli and the sphingosine kinase isoenzymes that are activated by allergens. The past years have provided increasing evidence that these processes contribute to pulmonary disorders including asthma, chronic obstructive pulmonary disease, acute lung injury, and cystic fibrosis. Sphingolipid metabolism offers several novel therapeutic targets for the treatment of lung diseases such as emphysema, asthma, cystic fibrosis, respiratory tract infection, sepsis, and acute lung injury.
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PMID:Sphingolipids in the lungs. 1875 26

The primary function of neutrophils in host defense is to contain and eradicate invading microbial pathogens. This is achieved through a series of swift and highly coordinated responses culminating in ingestion (phagocytosis) and killing of invading microbes. While these tasks are usually performed without injury to host tissues, in pathologic circumstances such as sepsis, potent antimicrobial compounds can be released extracellularly, inducing a spectrum of responses in host cells ranging from activation to injury and death. In the lung, such inflammatory damage is believed to contribute to the pathogenesis of diverse lung diseases, including acute lung injury and the acute respiratory distress syndrome, chronic obstructive lung disease, and cystic fibrosis. In these disorders, epithelial cells are targets of leukocyte-derived antimicrobial products, including proteinases and oxidants. Herein, we review the mechanisms involved in the physiologic process of neutrophil transepithelial migration, including the role of specific adhesion molecules on the leukocyte and epithelial cells. We examine the responses of the epithelial cells to the itinerant leukocytes and their cytotoxic products and the consequences of this for lung injury and repair. This paradigm has important clinical implications because of the potential for selective blockade of these pathways to prevent or attenuate lung injury.
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PMID:Transepithelial migration of neutrophils: mechanisms and implications for acute lung injury. 1897

Gc-globulin is a multifunctional glycoprotein with a molecular mass of 51-58 kDa. It is also called vitamin D-binding protein (DBP). The main function of Gc-globulin is to bind vitamin D and actin, which is released into the extracellular environment upon cell and tissue lysis. Gc-globulin appears to have important clinical significance. Some investigation have shown that a low concentration of Gc-globulin may be used as a prognostic factor in patients with fulminant hepatic failure, acetaminophen (paracetamol) overdose, multiple trauma or multiple organ dysfunction syndrome (MODS), or sepsis. Many studies suggest an association between Gc-globulin phenotypes and resistance or susceptibility to chronic obstructive pulmonary disease (COPD), thyroid diseases, diabetes, multiple sclerosis, and sarcoidosis.
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PMID:[The significance of Gc-globulin in clinical practice]. 1900 85

Ecthyma gangrenosum (EG) manifests as a skin lesion and is commonly associated with Pseudomonas aeruginosa septicemia in immunocompromised patients. Other viral, fungal and bacterial agents can also cause EG. The first clinical observation is grouped vesicles with surrounding erythema. Within a few days, they evolve into a gangrenous ulcer with a black/gray eschar surrounded by an erythematous halo. Herein, we present a patient with chronic obstructive pulmonary disease who developed EG-like lesions due to methicillin-resistant Staphylococcus aureus infection while he was in the intensive care unit.
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PMID:Ecthyma-gangrenosum-like lesions associated with methicillin-resistant Staphylococcus aureus infection. 1902 36

Common medical conditions that require mechanical ventilation include chronic obstructive lung disease, acute lung injury, sepsis, heart failure, drug overdose, neuromuscular disorders, and surgery. Although mechanical ventilation can be a life saving measure, prolonged mechanical ventilation can also present clinical problems. Indeed, numerous well-controlled animal studies have demonstrated that prolonged mechanical ventilation results in diaphragmatic weakness due to both atrophy and contractile dysfunction. Importantly, a recent clinical investigation has confirmed that prolonged mechanical ventilation results in atrophy of the human diaphragm. This mechanical ventilation-induced diaphragmatic weakness is important because the most frequent cause of weaning difficulty is respiratory muscle failure due to inspiratory muscle weakness and/or a decline in inspiratory muscle endurance. Therefore, developing methods to protect against mechanical ventilation-induced diaphragmatic weakness is important.
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PMID:Pressure support ventilation attenuates ventilator-induced protein modifications in the diaphragm. 1878 63

The first point of a good diagnostic strategy for healthcare-associated pneumonia (HCAP) is correct classification of patients with specific criteria, as suggested by the last American Thoracic Society/ Infectious Diseases Society of America (ATS/IDSA) guidelines. However, clinical practice and recent literature have suggested new risk factors for multidrug-resistant infection (MRI): the presence of permanent indwelling devices, prior antibiotic use in the last 3 months, chronic and advanced pulmonary diseases (chronic obstructive pulmonary disease, bronchiectasis, etc.), history of alcoholism, and immunosuppression. The clinical presentation in HCAP patients is often unusual (mild respiratory symptoms and frequent extrapulmonary manifestations) due to different factors: advanced age, neurological disorders, and multiple chronic comorbidities. Moreover, HCAP commonly presents a worse clinical course than community-acquired pneumonia, a prolonged length of stay, and a mortality rate close to hospital-acquired pneumonia. Chest radiography and routine laboratory markers (including C-reactive protein) are always needed for clinical evaluation and severity assessment. The clinical use of new biomarkers of infection and sepsis (procalcitonin, etc.) is currently being investigated. Extensive microbiological testing to overcome the high prevalence of MRI in HCAP, including urinary antigens for Legionella and Streptococcus pneumoniae; blood cultures; Gram staining and low respiratory tract secretions (sputum, tracheobronchial aspirate, fibrobronchial aspirate, protected specimen brush, bronchoalveolar lavage); and cultures for aerobic, anaerobic, mycobacterial, and fungal pathogens are recommended, whereas the indication for serology tests for respiratory viruses and atypical pathogens is low. By contrast, the new polymerase chain reaction-based techniques for the rapid identification (2 to 4 hours) of microbial pathogens in respiratory samples (nasopharyngeal swab, bronchoalveolar lavage) seem to be the most innovative future perspective in the diagnostics of HCAP.
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PMID:Diagnostic strategies for healthcare-associated pneumonia. 1919 85

Almost half of the hospitalized influenza patients have a chronic disease, which increases the risk for secondary bacterial infections and for adults >65 years influenza is related to high mortality risk. The impact of diabetes mellitus (DM), asthma bronchiale, cardiovascular disease (CVD) and chronic obstructive pulmonary disease (COPD) on the risk of having a low serum phosphatemia (S-P) in addition to influenza is important to investigate as this increases both morbidity and mortality and can be prevented. Hypophosphatemia could be the explanation for reduced chemo-taxis and phagocytosis, which in addition to respiratory function may increase the risk of pneumonia and sepsis. Data for this study was collected from the medical journals retrospectively for 100 patients admitted to the Department of Infectious Diseases during the study period, 1992-94, with the clinical diagnosis influenza out of which seventy-two cases were used in the calculation. Forty-seven percent of the hospitalized influenza patients had a 2.7-fold risk of suffering from DM than of any other chronic disease and an almost significantly doubled risk of having a low S-P level with a chronic disease. The prevalence of hypophosphatemia (S-P<0.70 mmol/l) was high; 13.0% of the women and 15.0% of the men; 34.0% of all patients had S-P<0.82 mmol/l. Men, in contrast to women, showed clinical signs of a secondary bacterial infection more frequently (12/41 and 6/35, respectively). Our study gives indications for an involvement of low S-P with chronic disease.
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PMID:Predisposing chronic diseases and hypophosphatemia in patients with influenza. 1964 May 97

Inflammation and immunity result in a wide range of disease processes, including chronic obstructive pulmonary disease, ischemia-reperfusion injury, atherosclerosis, vascular thrombosis and sepsis. Heme oxygenase-1 (HO-1) is a key enzyme that is indispensable for the temporal and spatial regulation of host response and, together with its essential metabolite carbon monoxide (CO), is crucial for maintaining homeostasis, inhibition of inflammation and the preservation of function and life. The biology of HO-1 is being discussed in this review series by Soares and colleagues and thus will not be reviewed here. Rather we will complement the HO-1 overview with a comprehensive discussion of CO as perhaps the one product of HO-1 that has been most studied. Of the numerous physiologic effects observed with CO, in the past five years it has become apparent that CO has been ascribed an additional novel role as a 'bactericidal agent'. Its role in the maintenance of homeostasis remains intact; however, the designation necessitates the paradoxical induction of the inflammatory response and binding to hemoproteins in order to restore homeostasis and sustain life. In this article, we review and discuss reports that have propelled and challenged the paradoxical use of CO, once viewed as a toxic molecule, now as a host defense molecule agent against microbes.
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PMID:Carbon monoxide is a poison... to microbes! CO as a bactericidal molecule. 1964 Jul 89


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