Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012739 (disseminated intravascular coagulation)
8,673 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A fluorochrome microassay was used to investigate peripheral blood polymorphonuclear leukocyte (PMNL) function in cattle. Glass-adherent PMNL were reacted with Staphylococcus aureus preincubated in 20% bovine serum for 30, 60 and 90 min. Coverslips were stained with acridine orange (AO) followed by crystal violet to quench extracellular bacterial fluorescence. PMNL function was evaluated by counting the number of dead (stained red with AO) and live (stained green with AO) S. aureus contained within 100 PMNL. A phagocytic index was calculated as the average number of bacteria contained within PMNL. The percentage killing of S. aureus was calculated from the average proportion of S. aureus within PMNL that were dead. Six clinically normal Holstein calves, 3-4 months of age, were sampled on 6 consecutive days. PMNL phagocytosis and killing did not vary significantly (p greater than 0.05) among repeated samplings per calf. PMNL function increased with increasing time of incubation of PMNL with S. aureus. Means (+/- SD) for percentage killing were 46.7 +/- 13.1, 57.4 +/- 11.6, and 62.1 +/- 9.8% for 30, 60 and 90 min of reaction, respectively. Means (+/- SD) for the phagocytic index were 2.9 +/- 0.8, 3.6 +/- 1.0, and 4.2 +/- 1.1 bacteria/PMNL for 30, 60 and 90 min of reaction, respectively. PMNL function was determined in 30 normal cattle of various breeds, age and sex, and these values were pooled to provide normal values for PMNL function. When values for bovine clinical patients (n = 25) with various diagnoses were compared with normal values (defined by the mean +/- 2SD for the 30 normal cattle) for PMNL function, only one patient was observed to exhibit PMNL hypofunction. A cow with disseminated intravascular coagulation in association with peracute coliform mastitis exhibited decreased PMNL killing capacity. Abnormal PMNL function was uncommon in the hospital population studied. Peripheral blood PMNL function was evaluated in lactating Holstein cows with (n = 15) or without (n = 15) chronic subclinical S. aureus mastitis. There was no significant (p greater than 0.05) difference in PMNL function among these cows.
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PMID:Polymorphonuclear neutrophil leukocyte function in clinical bovine patients and in cows with or without Staphylococcus aureus mastitis. 137 67

Gastric parietal cells in primary culture have been tested to determine their utility as a model for the study of the role of intracellular calcium ([Ca2+]i) in the control of HCl secretion. Changes in [Ca2+]i were measured in single cells on a microscope stage using the cell-permeant form of the fluorescent calcium probe, fura-2. Simultaneous images of cell fluorescence and morphology were acquired using a digitized video image analysis system and two video cameras, one for low-light level fluorescence detection and one for high resolution DIC/transmitted light images. Both histamine and carbachol, which are known stimulants of HCl secretion, increased [Ca2+]i and stimulated dramatic changes in morphology in these cultured cells. Changes in morphology were accompanied by an increased uptake of the weak base, [14C]-aminopyrine (AP), and a shift from green to red fluorescence of another weak base, acridine orange. These results indicate that cultured parietal cells, maintained under controlled conditions on a microscope stage, retain viability and secretagogue responsiveness. Thus, this cellular model appears to be suitable for correlation of changes in [Ca2+]i and activation of HCl secretion.
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PMID:HCl secretion and [Ca2+]i in cultured parietal cells. 238 25

Neutrophil-mediated oxidative stress on the rat mesenteric microcirculation was studied in the experimental model of endotoxin-induced disseminated intravascular coagulation (DIC) by using an intravital fluorescent technique and luminol-dependent chemiluminescence (ChL) analysis. Leukocytes sticking to the venules were visualized by the injection of acridine orange, a fluorochrome tracer which shows high affinity to white cells. Endotoxin (E coli, O-111B4, Difco, USA) was infused intravenously at a dose of 2 mg/kg/hr. After starting the infusion of endotoxin, the number of sticking cells were gradually increased on the venular endothelium followed by a transient neutropenia. In order to investigate the distribution of infused endotoxin in the microvasculature, FITC-labeled endotoxin (Sigma, USA) was used. After administration of FITC-endotoxin, multiple patches of fluorescence along the venular walls were observed, while no fluorescent conjugates were found at the sticking neutrophils and along the arteriolar walls. ChL activities of neutrophils were also dramatically elevated, which may reflect the enhanced ability to generate oxyradical species. To investigate the inhibitory effects of heparin sodium and gabexate mesilate which was a synthetic protease inhibitor on locomotive and metabolic changes of neutrophils induced by endotoxemia, both agents were administered prior to endotoxin infusion. Gabexate mesilate attenuated these changes, but heparin sodium did not show any improving effects. It was concluded that endotoxin primarily affects the venular endothelial cells, resulting in the activation of neutrophils. Gabexate mesilate was more likely to attenuate neutrophil-mediated oxidative stress on microvasculature in endotoxin-induced DIC than heparin sodium.
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PMID:Microcirculatory disturbances in endotoxin-induced disseminated intravascular coagulation. The effects of heparin and gabexate mesilate on locomotive and metabolic changes of neutrophils. 314 69

Neutrophil-mediated oxidative stress on the rat mesenteric microcirculation was studied in the experimental model of endotoxin-induced disseminated intravascular coagulation (DIC) by using an intravital fluorescent microscope equipped with a Silicon Intensifier Target Image Tube camera and luminol-dependent chemiluminescence (ChL) analysis. Leukocytes adhering to the venules were visualized by the injection of acridine orange, a fluorochrome tracer which shows high affinity to white cells. Endotoxin (E. coli, O-111 B4) was administered intravenously at a dose of 2 mg/kg/hour. After starting the infusion of endotoxin, the number of adherent cells gradually increased in the venular endothelium and was followed by a transient neutropenia. ChL activities from neutrophils were also significantly elevated, which may reflect the enhanced ability to generate oxygen-radicals. To elucidate the role of 5-lipoxygenase products in the locomotive and metabolic changes of neutrophils, the effects of AA-861, a specific inhibitor of 5-lipoxygenase was tested. In addition prednisolone and indomethacin were evaluated. AA-861 and prednisolone reduced neutropenia, leukocyte adhesion to the venular walls and ChL activities from neutrophils. It was concluded that 5-lipoxygenase may modulate neutrophil-mediated oxidative stress on microvasculature in endotoxin-induced DIC.
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PMID:5-lipoxygenase inhibitor (AA-861) attenuates neutrophil-mediated oxidative stress on the venular endothelium in endotoxemia. 338 68

Tissue thromboplastin generation in monocytes was studied during various stages of Escherichia coli endotoxinaemia in pigs. The pigs were monitored in halothane anaesthesia and mechanically ventilated. Blood was sampled from the superior caval vein before and during endotoxin infusion and up to 6 hours after its start. Monnuclear leukocytes were harvested with Lymphoprep separation and monocyte counts were made, using TRITC-labelled sheep erythrocytes, acridine orange and a fluorescence microscope. Thromboplastin was quantified in a two-stage assay by incubating the test sample together with purified factor X, factor VII and Ca++. The generated factor Xa was thereafter assayed. There was statistically significant increase of tissue thromboplastin activity in monocytes after endotoxin infusion. Maximum level was reached at the end of the infusion and was maintained throughout the observation period. Decrease occurred in platelets, leukocytes, antithrombin III, fibrinogen and clotting factors V, VII and VIII, and clotting time was prolonged. These findings indicated significant disseminated intravascular coagulation. The endotoxin-stimulated monocytes with their elevated tissue thrombo-plastin activity thus may play an important part in development of the DIC which so often follows septicemia.
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PMID:Tissue thromboplastin generation in circulating mononuclear phagocytes and development of coagulation disorders during E. coli endotoxinaemia in pigs. 392 66

Snow algae are photosynthetic microbes growing in thawing snow. They usually show various morphological cell types. The aim of this study was to carry out microscopic and spectroscopic analysis of different forms of cells of snow algae collected on glaciers in Alaska. Four different shapes of algal cells were observed with the use of bright field LM (Light Microscopy), DIC (Differential Interference Contrast), EDF (Extended Depth Focus), fluorescence microscopy, and SEM (Scanning Electron Microscopy). The cells exhibited the strongest autofluorescence after the exposure to 365-nm excitation light, and the intensity differed among the cell types. Zygotes (cysts) showed the most intense fluorescence. Acridine orange staining revealed the acid nature of the algal cells. The use of Congo red and Calcofluor white fluorochromes indicated differences in the structure of polysaccharides in the cell wall in the individual types of algal cells. FTIR (Fourier-Transform Infrared Spectroscopy) analyses showed the presence of polysaccharides not only in the algal cells but also in the fixative solution. The presence of polysaccharides in the extracellular algal fraction was confirmed by X-ray dispersion spectroscopy (EDS), X-ray photoelectron spectroscopy (XPS), and scanning electron microscopy imaging (SEM). The differences observed in the structure of the cell wall of the different forms of red snow algae prompt further analysis of this structure.
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PMID:Morphological and physicochemical diversity of snow algae from Alaska. 3315 22