Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Platelet vascular hemostasis was assessed in 32 patients with slight craniocerebral injuries (SCCI) (Glasgow coma score 14-15) (group 1) on days 1, 3, 5, and 7 and in 84 patients (score 3-8) (group 2) in the same terms and on days 9, 14, and 21 after the injury. Under study were platelet count, spontaneous platelet aggregation and that induced by ADP, adrenalin, and ristomicin. Moderate disorders of platelet vascular hemostasis were revealed in all the patients; they were most of all expressed on day 5 and were mainly due to moderate disorders of the athrombogenicity of the vascular endothelium. The injury caused a manifest dysfunction of platelets connected with the developing disseminated intravascular blood coagulation and, specifically, with injury to the vascular endothelium. Spontaneous aggregation of platelets was the maximum on day 5 and coincided in time with an increase in Willebrand factor-dependent ristomicin-induced platelet aggregation (Willebrand factor is a marker of injury to the vascular endothelium). An increase of ristomicin-induced platelet aggregation was more often observed in the patients who died than in the survivors, and in those developing the respiratory distress syndrome (stages II-IV) and that combined with pneumonia.
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PMID:[Thrombocytic hemostasis in patients with severe craniocerebral trauma]. 902 46

Inflammatory cell infiltration of the lung is a predominant histopathological change that occurs during radiation pneumonitis. Emigration of inflammatory cells from the circulation requires the interaction between cell adhesion molecules on the vascular endothelium and molecules on the surface of leukocytes. We studied the immunohistochemical pattern of expression of cell adhesion molecules in lungs from mice treated with thoracic irradiation. After X-irradiation, the endothelial leukocyte adhesion molecule 1 (ELAM-1; E-selectin) was primarily expressed in the pulmonary endothelium of larger vessels and minimally in the microvascular endothelium. Conversely, the intercellular adhesion molecule 1 (ICAM-1; CD54) was expressed in the pulmonary capillary endothelium and minimally in the endothelium of larger vessels. Radiation-mediated E-selectin expression was first observed at 6 h, whereas ICAM-1 expression initially increased at 24 h after irradiation. ICAM-1 and E-selectin expression persisted for several days. P-selectin is constitutively expressed in Weibel-Palade bodies in the endothelium, which moved to the vascular lumen within 30 min after irradiation. P-selectin was not detected in the pulmonary endothelium at 6 h after irradiation. The radiation dose required for increased cell adhesion molecule expression within the pulmonary vascular endothelium was 2 Gy, and expression increased in a dose-dependent manner. These data demonstrate that ICAM-1 and E-selectin expression is increased in the pulmonary endothelium following thoracic irradiation. The pattern of expression of E-selectin, P-selectin, and ICAM-1 is distinct from one another.
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PMID:Ionizing radiation mediates expression of cell adhesion molecules in distinct histological patterns within the lung. 918 1

Acute chest syndrome (ACS) is characterized by chest pain with dyspnea and recent radiologic abnormalities, and is an acute lung complication whose problem is one of etiology. Alveolar hypoventilation linked to infarcts of the thoracic ribs, thoracoabdominal trauma, subdiaphragmatic pain, the administration of analgesics causing respiratory depression, or sleep disturbance, is a frequent cause of ACS. Bronchoalveolar lavage has revealed the frequency of fat embolism following infarcts in the long bones. Pulmonary vascular occlusion, due to thrombosis or emboli, is rare, as are the infectious pneumonia and pulmonary edema. The pathogenetic mechanisms consist of an alteration of the rheological properties of the blood, the existence of an hypercoagulability state, specific interactions between the abnormal sickle cells and the vascular endothelium, and a dysregulation of the vascular reactivity. Research centered around NO biology has led to an expanded understanding of the critical interdependence of NO, hemoglobin, and the microvasculature. An anemic patient with ACS suffers from loss of pulmonary scavenging and hypoxic pulmonary vasoconstriction and loss of peripheral NO delivery. Interruption of this cycle by transfusing normal (hemoglobin A-containing) erythrocytes might improve all the abnormalities.
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PMID:[Respiratory distress and drepanocytosis]. 1079 55

This study focuses on a possible role of intercellular adhesion molecule-1 (ICAM-1) in interstitial pulmonary diseases. We determined a soluble form of ICAM-1 in serum and bronchoalveolar lavage fluid (BALF) using ELISA in patients with usual interstitial pneumonia (UIP), bronchiolitis obliterance organizing pneumonia (BOOP), or nonspecific interstitial pneumonia (NSIP). In addition, we investigated the expression of ICAM-1 in the lung tissues of these patients by means of immunohistochemical staining. Serum levels of soluble ICAM-1 were significantly higher in patients with UIP or NSIP than in healthy subjects, and were also high in patients with BOOP. The soluble ICAM-1 in BALF tended to be higher in patients with UIP, BOOP, or NSIP than in normal subjects. A significant correlation was seen between soluble levels of ICAM-1 in serum and BALF. In the immunostaining of ICAM-1 of the lung tissues, ICAM-1 expression was more pronounced in patients with UIP than in those with BOOP or NSIP. The increased expression of ICAM-1 was seen in type II alveolar epithelium and vascular endothelium in patients with interstitial pneumonia. A positive correlation was observed between the degree of ICAM-1 expression in the lung tissues and the BALF levels of soluble ICAM-1. The expression of ICAM-1 in type II alveolar epithelium suggests that ICAM-1 plays a specific role in the fibrotic process of the lung, and that the measurement of soluble ICAM-1 in sera and BALF could be a useful marker for evaluating the progression of fibrosis.
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PMID:Intercellular adhesion molecule-1 in patients with idiopathic interstitial pneumonia. 1151 62

Mice infected with K. pneumoniae against the background of prior introduction of influenza A/Hong-Kong/68 virus developed focal bronchial pneumonia with leukocytic exudate that started resolving at day 10 of the experiment. At about this time and later there appeared in the lungs spots of apparent proliferative processes characteristic of productive inflammation. These were manifested by diffuse and focal infiltration of the interstice with plasmablasts, plasmacytes, histiocytes, lymphocytes, by proliferation of the vascular endothelium epithelium, of the bronchi, bronchioles, alveolar cells that were seen to be desquamative and developing obliterating macrophagal alveolitis, focal proliferation of fibroblasts. Abnormalities in immunoregulatory mechanisms were induced by immunodepressive action of the influenza virus, early chronization of viral-bacterial pneumonia, with pneumosclerosis developing in its wake.
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PMID:[Pathomorphological aspects and outcome of influenza virus and Klebsiella pneumonia in the experiment]. 1531 7

Mycoplasma bovis can cause arthritis or mastitis following pneumonia and mycoplasmemia in cattle. Interactions with pulmonary vascular endothelium have been recorded as localized vasculitis, perivascular mononuclear cell infiltrations, and accumulation of inflammatory cells in lesions. We compared adhesion mediators and cytokine gene expression as well as cytotoxicity of cultured primary bovine aortic and bovine pulmonary microvascular endothelial cells (BPMEC) challenged with M. bovis. We also tested if abscess-forming ability of strains of M. bovis is associated with changes on endothelial cells. Increased VCAM-1 surface expression was found in both cell types, while only infected BPMEC increased MCP-1 transcription, both mediators specific for mononuclear cell transmigration. Given no induction of ICAM-1 mRNA in either cell type, induction of IL-8 mRNA by BPMEC suggested that neutrophil transmigration was signaled in microvascular areas. Infected BPMEC showed early induction of IL-1beta and IL-6 mRNA. Excepting VCAM-1, differential strain effects were limited to BPMEC and not correlated with their abscess-forming capability. In addition, only strain DSA16 had minor cytotoxic effect on both cell types. We thus show that BPMEC are more susceptible than aortic cells to M. bovis-induced activation. Activation preferentially yielded signals for mononuclear cell transmigration, correlating well with in vivo observations of infiltrating cells at pulmonary sites.
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PMID:Endothelial cells from bovine pulmonary microvasculature respond to Mycoplasma bovis preferentially with signals for mononuclear cell transmigration. 1551 46

8 patients, aged from 61 to 70 years, died from serous meningoencephalitis during the outburst of the West Nile fever in Volgograd in 1999-2001, were studied morphologically. Serous meningoencephalitis with necrotic vasculitis is a characteristic feature of this fever with degenerative changes and destructive foci in the brain. Proteinic and fatty inflammatory and lymphomacrophageal reactions were observed in the liver, serous productive myocarditis and cardiomyocytic necrosis dystrophy. Desquamative pneumonia, intracapillary nephritis were also seen. Immunohistochemical reaction against virus of this fever was positive in the vascular endothelium of parenchymal organs, hepatocytes, neurons of the brain.
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PMID:[Pathomorphology of West Nile fever]. 1557 79

The purpose of the study was to investigate the vasomotor and NO-production functions of the endothelium (VFE and NOPFE) in patients with extrahospital pneumonia (EHP) of various severity. 60 patients with EHP of various severity, aged 18 to 35 years, were examined. VFE was studied by ultrasonic method (SonoLine Versa Plus, Siemens, Germany) using reactive hypermia test. NOPFE was investigated by measuring total level of NO metabolites by calorimetric method using Griess reagent. The total oxidative and total anti-oxidative activity (TOA, TAOA) in serum was determined. The study revealed functional disturbances of the vascular endothelium at the culmination of EHP. In cases of severe EHP there was insufficient vasodilatation and even vasoconstriction within the 1st minute after reactive hyperthermia test. During the recovery period the parameters were the same as in the patients of the control group. In cases of mild and moderate EHP moderate vasomotor dysfunction was observed, which was not seen during the recovery period. At the culmination of severe EHP NOPFE dysfunction was observed, which manifested by substantial decrease of basal NO secretion and low NO-reactivity of the endothelium (NORE). In cases of mild and moderate EHP low NORE and normal basal level of NO metabolites were seen. During the recovery period NORE returned to its normal level. The patients displayed TOA/TAOA disbalance in serum. There is a significant correlation between TOA/TAOA balance and the functional condition of the endothelium in patients with EHP. Thus, the study revealed endothelial dysfunction, which was strongly associated with the severity of the disease. TOA/ TAOA disbalance is a potential mechanism of endothelial dysfunction in patients with EHP.
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PMID:[Functional condition of the vascular endothelium in patients with extrahospital pneumonia]. 1611 19

Angiosarcoma of the temporal bone is an extremely rare malignant tumor, which originates from vascular endothelium. We describe a case of a 57-year-old woman, initially presenting with progressive hearing loss, otorrhea as well as facial palsy diagnosed as a mastoiditis elsewhere. After subtotal mastoidectomy histological examination revealed an angiosarcoma of the mastoid. Since the tumor was not completely removed lateral petrosectomy and postoperative radiotherapy were performed. Afterwards the patient developed local recurrence with intracerebral tumor extension. During palliative polychemotherapy the patient developed a pneumonia and deceased. In this manuscript the morphology, imaging characteristics and current treatment options of angiosarcomas of the lateral skull base are reviewed and discussed.
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PMID:[Angiosarcoma of the temporal bone]. 1850 95

Porcine circovirus 2 (PCV2) is the primary causative agent of porcine circovirus disease (PCVD). PCVD is an emerging disease that has been reported worldwide, associated with wasting, lymphoid depletion, enteritis, pneumonia, vasculitis, ischemic lesions, and necrotizing dermatitis. Although PCVD causes considerable economic losses, the pathogenesis of PCV2 has not been fully understood. The aim of the present work was to study the participation of hemostatic system and of vascular endothelium in PCV2 infection, as well as their possible role in PCVD pathogenesis. Our results showed that naturally PCV2-infected swine displayed a prothrombotic state in vivo, since a diminished coagulation time (recalcification time, activated partial thromboplastin time and prothrombin time), a higher platelet aggregation ability (despite a diminished platelet blood count), and an increased thrombin plasma activity (associated with a reduced fibrinogen level) were observed. The PCV2-infected animals showed vasculitis and positive staining for PCV2 antigen in capillary vessels. Furthermore, PCV2-infected endothelial cells displayed an activated phenotype, characterized by an increase in cell surface procoagulant activity. Moreover, the PCV2-infected endothelial cells pre-treated with exogenous thrombin displayed an increased viral load. This work reports, for the first time, the role of the hemostatic system and of endothelium in the pathogenesis and infectivity of PCV2. The study reinforces the importance of the phenomena which occur during PCV2 infection, and affords a better knowledge of the mechanisms behind the pathophysiology of PCVD.
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PMID:Porcine circovirus 2 (PCV2) induces a procoagulant state in naturally infected swine and in cultured endothelial cells. 1973 20


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