An evaluation of the role of leukocytes in the pathogenesis of experimentally induced corneal vascularization.
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Studies of corneal explants in the hamster cheek pouch chamber have demonstrated that blood vessels invade the cornea only if the tissue is first infiltrated by leukocytes. In view of this observation, a comparative study of the events that precede and accompany corneal vascularization was undertaken in various experimental models. A variety of established methods were used to induce corneal vascularization, including exposure of the cornea to noxious agents, intracorneal injection of antigens into sensitized animals, as well as maintaining animals on diets deficient in vitamin A or riboflavin. In all models studied, the corneal vascularization was a manifestation of the reparative phase of the inflammatory response. A conspicuous leukocytic infiltrate of the cornea preceded and accompanied the corneal vascularization in all of the models. Although the lesions varied in several respects in the different models, all models displayed three phases with regard to vascularization: an early prevascular phase of leukocytic infiltration, a second phase where blood vessels persisted in the cornea in the absence of leukocytes. The latent period that preceded vascularization was directly related to the time of the initial leukocytic infiltration. The models in which a delay occurred in the leukocytic invasion displayed a subsequent delay in the vascular ingrowth. Conversely, in experiments where there was a rapid and extensive leukocytic invasion, there was also an early and enhanced corneal vasoproliferative response. In the various modesl investigated, the sites of the leukocytic infiltration and subsequent vascular ingrowth into the cornea paralleled each other. The data further support the hypotheses that leukocytes are a prerequisite to corneal vascularization and that leukocytes produce one or more factors which stimulate directional vascular growth. (+info)
Survival and heat resistance of Listeria monocytogenes after exposure to alkali and chlorine.
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A strain of Listeria monocytogenes isolated from a drain in a food-processing plant was demonstrated, by determination of D values, to be more resistant to the lethal effect of heat at 56 or 59 degrees C following incubation for 45 min in tryptose phosphate broth (TPB) at pH 12.0 than to that of incubation for the same time in TPB at pH 7.3. Cells survived for at least 6 days when they were suspended in TPB at pHs 9.0, 10.0, and 11.0 and stored at 4 or 21 degrees C. Cells of L. monocytogenes incubated at 37 degrees C for 45 min and then stored for 48 or 144 h in TPB at pH 10.0 were more resistant to heat treatment at 56 degrees C than were cells stored in TPB at pH 7.3. The alkaline-stress response in L. monocytogenes may induce resistance to otherwise lethal thermal-processing conditions. Treatment of cells in 0.05 M potassium phosphate buffer (pH 7.00 +/- 0.05) containing 2.0 or 2.4 mg of free chlorine per liter reduced populations by as much as 1.3 log(10) CFU/ml, while treatment with 6.0 mg of free chlorine per liter reduced populations by as much as 4.02 log(10) CFU/ml. Remaining subpopulations of chlorine-treated cells exhibited some injury, and cells treated with chlorine for 10 min were more sensitive to heating at 56 degrees C than cells treated for 5 min. Contamination of foods by L. monocytogenes cells that have survived exposure to processing environments ineffectively cleaned or sanitized with alkaline detergents or disinfectants may have more severe implications than previously recognized. Alkaline-pH-induced cross-protection of L. monocytogenes against heat has the potential to enhance survival in minimally processed as well as in heat-and-serve foods and in foods on holding tables, in food service facilities, and in the home. Cells surviving exposure to chlorine, in contrast, are more sensitive to heat; thus, the effectiveness of thermal processing in achieving desired log(10)-unit reductions is not compromised in these cells. (+info)
Lack of degradation of sevoflurane by a new carbon dioxide absorbent in humans.
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BACKGROUND: Potent inhaled anesthetics degrade in the presence of the strong bases (sodium hydroxide or potassium hydroxide) in carbon dioxide (CO2) absorbents. A new absorbent, Amsorb (Armstrong Medical Ltd., Coleraine, Northern Ireland), does not employ these strong bases. This study compared the scavenging efficacy and compound A production of two commercially available absorbents (soda lime and barium hydroxide lime) with Amsorb in humans undergoing general anesthesia. METHODS: Four healthy volunteers were anesthetized on different days with desflurane, sevoflurane, enflurane, and isoflurane. End-tidal carbon dioxide (ETCO2) and anesthetic concentrations were measured with infrared spectroscopy; blood pressure and arterial blood gases were obtained from a radial artery catheter. Each anesthetic exposure lasted 3 h, during which the three fresh (normally hydrated) CO2 absorbents were used for a period of 1 h each. Anesthesia was administered with a fresh gas flow rate of 2 l/min of air:oxygen (50:50). Tidal volume was 10 ml/kg; respiratory rate was 8 breaths/min. Arterial blood gases were obtained at baseline and after each hour. Inspired concentrations of compound A were measured after 15, 30, and 60 min of anesthetic administration for each CO2 absorbent. RESULTS: Arterial blood gases and ETCO2 were not different among three CO2 absorbents. During sevoflurane, compound A formed with barium hydroxide lime and soda lime, but not with Amsorb. CONCLUSIONS: This new CO2 absorbent effectively scavenged CO2 and was not associated with compound A production. (+info)
Systemic and local effects of long-term exposure to alkaline drinking water in rats.
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Alkaline conditions in the oral cavity may be caused by a variety of stimuli, including tobacco products, antacids, alkaline drinking water or bicarbonate toothpaste. The effects of alkaline pH on oral mucosa have not been systematically studied. To assess the systemic (organ) and local (oral mucosal) effects of alkalinity, drinking water supplemented with Ca(OH)2 or NaOH, with pH 11.2 or 12 was administered to rats (n = 36) for 52 weeks. Tissues were subjected to histopathological examination; oral mucosal biopsy samples were also subjected to immunohistochemical (IHC) analyses for pankeratin, CK19, CK5, CK4, PCNA, ICAM-1, CD44, CD68, S-100, HSP 60, HSP70, and HSP90. At completion of the study, animals in the study groups had lower body weights (up to 29% less) than controls despite equal food and water intake, suggesting a systemic response to the alkaline treatment. The lowest body weight was found in rats exposed to water with the highest pH value and starting the experiment when young (6 weeks). No histological changes attributable to alkaline exposure occurred in the oral mucosa or other tissues studied. Alkaline exposure did not affect cell proliferation in the oral epithelium, as shown by the equal expression of PCNA in groups. The up-regulation of HSP70 protein expression in the oral mucosa of rats exposed to alkaline water, especially Ca(OH)2 treated rats, may indicate a protective response. Intercellular adhesion molecule-1 (ICAM-1) positivity was lost in 6/12 rats treated with Ca(OH)2 with pH 11.2, and loss of CD44 expression was seen in 3/6 rats in both study groups exposed to alkaline water with pH 12. The results suggest that the oral mucosa in rats is resistant to the effects of highly alkaline drinking water. However, high alkalinity may have some unknown systemic effects leading to growth retardation, the cause of which remains to be determined. (+info)
Molecular analysis of a carbohydrate antigen involved in the structure and function of zona pellucida glycoproteins.
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A lactosaminoglycan-associated antigen is associated with a carbohydrate moiety of all three zona pellucida (ZP) glycoproteins of pig and rabbit but is absent in the mouse and rat. A monoclonal antibody (PS1) recognizing this determinant was obtained by immunizing mice with a porcine ZP glycoprotein isoform purified by two-dimensional polyacrylamide gel electrophoresis. Conditions known to remove O-linked or sialic acid carbohydrate moieties (alkaline reduction; O-glycanase or neuraminidase enzymatic cleavage) did not remove the carbohydrate epitope. However, treatment with endo-beta-glycosidase, endoglycosidase F, or combinations of neuraminidase plus beta-galactosidase, totally removed the determinant, indicating that it is associated with a poly-N-acetyllactosaminoglycan structure present on an N-linked oligosaccharide. Molecular morphology studies using immunofluorescence and confocal microscopy techniques demonstrate that the PS1 antigen is localized at the surface of the ZP. Confirmation of this localization was obtained through studies that show that this antibody will inhibit homologous sperm binding to the pig ZP. Additional analyses using modular contrast microscopy and immunocytochemistry demonstrate that this carbohydrate-associated antigen is localized in discrete layers throughout the ZP matrix. These studies are the first to demonstrate the presence of a lactosaminoglycan type carbohydrate moiety in all three ZP proteins using a monoclonal antibody that appears to be involved in sperm recognition and structural organization. (+info)
Compound A production from sevoflurane is not less when KOH-free absorbent is used in a closed-circuit lung model system.
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In an in vitro study, less compound A was formed when a KOH-free carbon dioxide absorbent was used. To confirm this observation we used a lung model in which carbon dioxide was fed in at 160 ml min(-1) and sampling gas was taken out for analysis at 200 ml min(-1); ventilation aimed for a PE'CO2 of 5.4 kPa. The soda lime canister temperatures in the inflow and outflow ports (Tin and Tout) were recorded. In six runs of 240 min each, a standard soda lime, Sodasorb (Grace, Epernon, France) was used and in eight runs KOH-free Sofnolime (Molecular Products, Thaxted, UK) was used. Liquid sevoflurane was injected using a syringe pump to obtain 2.1% E'. Compound A was measured by capillary gas chromatography combined with mass spectrometry. Median (range) compound Ainsp increased to a maximum of 22.7 (7.9) ppm for Sodasorb and 33.1 (20) for Sofnolime at 60 min and decreased thereafter; the difference between groups was significant (P<0.05) at each time of analysis up to 240 min. The canister temperatures were similar in both groups and increased to approximately 40 degrees C at 240 min. Contrary to expectation, compound A concentrations were greater with the KOH-free absorbent despite similar canister temperatures with both absorbents. (+info)
Evaluation of BacT/Alert 3D liquid culture system for recovery of mycobacteria from clinical specimens using sodium dodecyl (lauryl) sulfate-NaOH decontamination.
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A total of 52 mycobacterial isolates were recovered from 1,197 clinical specimens decontaminated by a sodium dodecyl (lauryl) sulfate (SDS)-NaOH protocol. Of these, 94% were recovered with the BacT/Alert 3D system (Organon Teknika, Durham, N.C.) and 79% were recovered on Lowenstein-Jensen (LJ) medium. Mean times to detection of organisms of the Mycobacterium tuberculosis complex (n = 47) were 22.8 days with LJ medium and 16.2 days with the system. The BacT/Alert 3D system is a rapid and efficient detection system which can be used with an SDS-NaOH decontamination procedure. (+info)
Only carbon dioxide absorbents free of both NaOH and KOH do not generate compound A during in vitro closed-system sevoflurane: evaluation of five absorbents.
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BACKGROUND: Insufficient data exist on the production of compound A during closed-system sevoflurane administration with newer carbon dioxide absorbents. METHODS: A modified PhysioFlex apparatus (Drager, Lubeck, Germany) was connected to an artificial test lung (inflow at the top of the bellow approximately/= 160 ml/min CO2; outflow at the Y piece of the lung model approximately/= 200 ml/min, simulating oxygen consumption). Ventilation was set to obtain an end-tidal carbon dioxide partial pressure of approximately 40 mmHg. Various fresh carbon dioxide absorbents were used: Sodasorb (n = 6), Sofnolime (n = 6), and potassium hydroxide (KOH)-free Sodasorb (n = 7), Amsorb (n = 7), and lithium hydroxide (n = 7). After baseline analysis, liquid sevoflurane was injected into the circuit by syringe pump to obtain 2.1% end-tidal concentration for 240 min. At baseline and at regular intervals thereafter, end-tidal carbon dioxide partial pressure, end-tidal sevoflurane concentration, and canister inflow (T degrees(in)) and canister outflow (T degrees(out)) temperatures were measured. To measure compound Ainsp concentration in the inspired gas of the breathing circuit, 2-ml gas samples were taken and analyzed by capillary gas chromatography plus mass spectrometry. RESULTS: The median (minimum-maximum) highest compound Ainsp concentrations over the entire period were, in decreasing order: 38.3 (28.4-44.2)* (Sofnolime), 30.1 (23.9-43.7) (KOH-free Sodasorb), 23.3 (20.0-29.2) (Sodasorb), 1.6 (1.3-2.1)* (lithium hydroxide), and 1.3 (1.1-1.8)* (Amsorb) parts per million (*P < 0.01 vs. Sodasorb). After reaching their peak concentration, a decrease for Sofnolime, KOH-free Sodasorb, and Sodasorb until 240 min was found. The median (minimum-maximum) highest values for T degrees(out) were 39 (38-40), 40 (39-42), 41 (40-42), 46 (44-48)*, and 39 (38-41) degrees C (*P < 0.01 vs. Sodasorb), respectively. CONCLUSIONS: With KOH-free (but sodium hydroxide [NaOH]-containing) soda limes even higher compound A concentrations are recorded than with standard Sodasorb. Only by eliminating KOH as well as NaOH from the absorbent (Amsorb and lithium hydroxide) is no compound A produced. (+info)