Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:A7KAX9 (grit)
 1,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among the waterfowl affected by white phosphorus (P4) at a military base in Alaska are tundra (Cygnus columbianus) and trumpeter (C. buccinator) swans. To estimate the toxicity of P4 to swans and compare the toxic effects to those of mallards (Anas platyrhynchos), we dosed 30 juvenile mute swans (C. olor) with 0 to 5.28 mg P4/kg body weight. The calculated LD50 was 3.65 mg/kg (95% CI: 1.40 to 4. 68 mg/kg). However, many of the swans still had P4 in their gizzards after dying, as determined by "smoking gizzards" and characteristic odor, and a lower LD50 might be calculated if all of the P4 had passed into the small intestines. We attribute the retention of P4 in swans to the possibility that P4 pellets were mistaken for the similarly sized grit in their gizzards. Most swans took 1 to 4.5 days to die in contrast to the few hours normally required in mallards and death appeared to be related more to liver dysfunction than to hemolysis. White phosphorus affected several plasma constituents, most notably elevated aspartate aminotransferase, blood urea nitrogen, lactate dehydrogenase, and alanine aminotransferase.
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PMID:Acute toxicity and sublethal effects of white phosphorus in mute swans, Cygnus olor. 1004

Endosseous implants initially come into contact with blood. Thus, the nature of the interactions between blood and implanted endosseous implants may influence subsequent bone healing events in the peri-implant healing compartment. We conducted studies to address the following question: Does implant surface microtexture modulate platelet activity? We used commercially pure Ti (cpTi) disks with four different surface finishes: dual acid-etched (DAE), 320 grit (320G) abraded, machined, and p1200 polished cpTi. Surfaces were characterized by scanning electron microscopy (SEM) and optical profilometry. The DAE and 320G surfaces presented more complex microtextures than the machined or polished surfaces. Platelet activities were measured by quantifying platelet adherence, platelet-derived microparticle (MP) formation, and P-selectin expression as function of surface type. Platelet adhesion, measured using a lactate dehydrogenase (LDH) assay. was increased on DAE and 320G surfaces compared to machined and polished surfaces (p < 0.05). M P formation and P-selectin expression, assayed by flow cytometry, also showed increased activation of platelets on DAE and 320G surfaces. Because increased activation of platelets may lead to up-regulation of osteogenic responses during bone healing, these results may explain the enhanced osteoconductivity known to occur with DAE cpTi surfaces in comparison with machined cpTi surfaces.
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PMID:Platelet interactions with titanium: modulation of platelet activity by surface topography. 1151 87

Blasting sand is used for abrasive blasting, but its inhalation is associated with pulmonary inflammation and fibrosis. Consequently, safer substitute materials for blasting sand are needed. In a previous study from this laboratory, the comparative pulmonary toxicity of five abrasive blasting substitutes and blasting sand was reported. In this study, the pulmonary toxicity of blasting sand was compared to five additional abrasive blasting substitutes: steel grit, copper slag, nickel slag, crushed glass, and olivine. Exposed rats received by intratracheal instillation 10 mg of respirable-size particles of blasting sand or an abrasive blasting substitute, while controls were instilled with vehicle. Pulmonary inflammation, damage, and fibrosis were examined 28 d postexposure. Pulmonary inflammation was monitored by determining bronchoalveolar lavage polymorphonuclear cell counts and alveolar macrophage activation by chemiluminescence. Pulmonary damage was assessed by acellular bronchoalveolar (BAL) fluid serum albumin concentrations and lactate dehydrogenase activities. Histological examination of lung tissue samples was made to assess the severity and distribution of pulmonary fibrosis, alveolitis, and alveolar epithelial cell hypertrophy and hyperplasia. In comparison to blasting sand, olivine exposed rats had higher levels of pulmonary inflammation and damage with a similar level of fibrosis. Steel grit-exposed rats had lower levels of pulmonary inflammation and damage, and did not develop fibrosis. However, steel grit-exposed rats had a level of epithelial cell hypertrophy and hyperplasia similar to blasting sand. The other abrasive blasting substitutes gave a mixed profile of toxicity. The data demonstrate that steel grit produced less acute pulmonary toxicity than blasting sand or any of the other abrasive blasting substitutes. Notwithstanding, the data also suggest that chronic exposure to steel grit may pose a health risk due to its effects on epithelial cell proliferation in the lung.
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PMID:Comparative pulmonary toxicity of blasting sand and five substitute abrasive blasting agents. 1216 12