Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
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Diopside ceramic pellets with a nominal composition of 55.5 wt % SiO(2)-25.9 wt % CaO-18.0 wt % MgO were soaked in human parotid saliva (HPS) over different time intervals, to investigate the behavior of the material in a natural medium of high protein content. The results showed the formation of a hydroxyapatite (HA)-like layer on the surface of the ceramic, and suggested that the mechanism of HA-like layer formation in saliva was similar to that showed in vitro test by other silica-based materials. The HA-like layer formed at the interface was found to be compact, continuous, and composed of many small crystallites with ultrastructure similar to that of natural cortical bone and dentine. The study concluded that the high pH conditions (9.8) existing right at the ceramic/human parotid saliva interface promoted HA-like phase precipitation. At this stage of the study, it is possible to suggest that the diopside ceramic could be of interest in specific periodontal applications for bone restorative purposes. Morphology, structure, and composition of the interfacial reaction product were examined by Scanning and Transmission Electron Microscopy techniques (SEM and TEM), combined with Energy Dispersive X-say Spectroscopy (EDS). Changes in ionic concentrations were measured using Inductively Coupled Plasma Atomic Emission Spectroscopy (ICP-AES), while the pH right at the interface of diopside/PHS were determined with an Ion Sensitive Field Effect Transistor (ISFET-Meter) instruments.
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PMID:Bioactivity of diopside ceramic in human parotid saliva. 1573 73

Previous studies demonstrated that bacterial lipopolysaccharide (LPS, endotoxin) triggers pulmonary vasoconstriction leading to pulmonary hypertension (PHS, ascites) in broilers. The lungs of broilers are constantly challenged with LPS that can trigger pulmonary vasoconstriction. Among broilers from a single genetic line, some individuals respond to LPS with large increases in pulmonary arterial pressure (PAP), whereas others fail to exhibit any response to the same supramaximal dose of LPS. In the present study we evaluated the impact of a variety of factors on the magnitude of the PAP response of male broilers to LPS, including: (1) the role of the initial PAP (low vs. high initial PAP); (2) the source of the LPS (Salmonella typhimurium vs. Escherichia coli); (3) the dose of LPS (0.02, 0.1, and 0.5 mg/kg of BW); and (4) the role of micro-particle selection for improved pulmonary vascular capacity (cellulose survivors vs. saline-injected controls). Broilers in the low initial PAP group (21 +/- 0.34 mmHg, mean +/- SEM) did not differ in their pulmonary hypertensive response to LPS compared with broilers in the high initial PAP group (29 +/- 0.55 mmHg, mean +/- SEM). Lipopolysaccharide from S. typhimurium elicited pulmonary hypertensive responses qualitatively similar to those elicited by E. coli LPS. A detailed evaluation revealed that an LPS dose of 0.1 mg/kg of BW elicits a maximal pulmonary hypertensive response in male broilers, and broilers selected by micro-particle injection for a robust pulmonary vascular capacity did not differ in their pulmonary hypertensive response to LPS compared with unselected broilers. This research confirms that the variable pulmonary hypertensive responses among broilers cannot be attributed to the source or dosage of LPS, or to differences in the baseline pulmonary arterial pressure or micro-particle selection before injecting LPS. These findings are consistent with the hypothesis that innate rather than acquired variability may influence the profile of chemical mediators released during the inflammatory cascade.
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PMID:Pulmonary hypertensive responses of broilers to bacterial lipopolysaccharide (LPS): evaluation of LPS source and dose, and impact of pre-existing pulmonary hypertension and cellulose micro-particle selection. 1578 12