Cystolithiasis secondary to intravesical foreign body in a horse.
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Animals↗
Biomedical subjects
J A Textor
Publications and source records attributed to J A Textor.
Umbilical evagination of the urinary bladder in a neonatal filly.
An 8-hour-old Standardbred filly was evaluated because of an enlarging umbilical mass and stranguria. It was suspected that the mass was the urinary bladder; this was confirmed on surgical exploration of the abdomen. Despite a normal umbilical ring, the bladder had descended and partially everted through its urachal communication with the umbilical stalk. Partial cystectomy and umbilical resection were performed and resulted in an excellent clinical outcome. Evagination of the urinary bladder via the umbilicus has rarely been described in human infants, and, to our knowledge, it has not been reported in the veterinary literature.
Animals↗
Subchondral cystic lesions of the proximal extremity of the tibia in horses: 12 cases (1983-2000).
OBJECTIVE: To determine clinical and radiographic features of subchondral cystic lesions (SCL) of the proximal extremity of the tibia in horses that could be used to classify these lesions as being related to osteochondrosis or osteoarthritis and to evaluate results of surgical debridement. DESIGN: Retrospective study. ANIMALS: 12 horses with 14 SCL. PROCEDURE: Medical records and radiographs obtained before and after treatment were reviewed. RESULTS: In 6 young horses (8 lesions), SCL were considered to be related to osteochondrosis; all involved the lateral tibial condyle. The remaining 6 horses were mature and had radiographic evidence of osteoarthritis in addition to SCL. Arthroscopic debridement was performed in 4 horses in which lesions were considered to be a result of osteochondrosis and in 3 horses with osteoarthritis. Three horses in which SCL were considered to be a result of osteochondrosis performed athletically after debridement. Two horses with moderate osteoarthritis returned to work after arthroscopic debridement but at a lower level of athletic performance. One horse with SCL related to osteochondrosis responded to medical treatment and went on to race. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that arthroscopic debridement of SCL is feasible in horses in which lesions involve the cranial portion of the lateral or medial tibial condyle, and that treated horses may be able to perform athletically.
Animals↗
Expression and characterization of the human erythrocyte anion exchanger in a baculovirus/Sf-9 cell system.
The human erythrocyte anion-exchange protein (HAE1) has been expressed in insect Sf-9 cells using a recombinant baculovirus. We subcloned the full-length cDNA encoding HAE1 into the baculovirus expression vector pVL1392 and cotransfected Sf-9 cells with the recombinant vector and wild-type AcMNPV DNA to obtain recombinant baculovirus. The expressed protein was targeted to the Sf-9 plasma membrane at an apparent density of approximately 0.5 x 10(6) copies/cell as determined by quantitative autoradiography using an HAE1-specific monoclonal antibody. Unlike native HAE1, the expressed protein was not glycosylated. Transport studies with HAE1-recombinant-infected Sf-9 cells showed saturable [Km(Cl-) = 44 mM; Vmax(Cl-) = 48 mEq/liter of cell waters min] and H2DIDS-inhibitable (K(O.5) = 34 microM) 36Cl- uptake that was not present in uninfected cells. We also found that extracellular SO4(2-) reduced 36Cl- influx [K(0.5)((SO4)2-) = 26 mM], presumably through substrate competition as in erythrocytes. Finally, we observed that H2DIDS-inhibitable 36Cl- efflux was reduced by 77% in the nominal absence of a suitable counter-anion in the external solution (HCO3(-)-free, all-glucuronate medium), thereby providing strong evidence for an obligatory exchange mechanism. We conclude that there is high-level expression of + ++HAE1 functional activity in recombinant baculovirus-infected Sf-9 cells and that this system will prove useful for kinetic and structural analyses of the HAE1 protein.
4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
Cell volume regulation in human neutrophils: 2-(aminomethyl)phenols as Cl- channel inhibitors.
When subjected to hypotonic stress, human peripheral neutrophils initially swell due to rapid water entry and thereafter recover toward the normal cell size (approximately 330 microns 3). Neutrophils do not behave as perfect osmometers: when resuspended in half-isotonic medium (150 mosM), they swell by only approximately 40% rather than doubling in size as predicted for ideal behavior. As with lymphocytes, restoration to the normal cell size involves the net loss of K+ and Cl- from the cytosol through independent conductance pathways. Volume regulation is sensitive to 0.4-1 mM of quinine, UK-5099, 3,5-diiodosalicylate (DISA), MK-473 (an indanyloxyacetate derivative), and to MK-447 [a 2-(aminomethyl)phenol]. From correlation of drug effects on the time course of cell volume recovery and the associated volume-activated 86Rb+ and 36Cl- fluxes, it was evident that quinine blocked only K+ channels, whereas MK-447 acted as a selective inhibitor of Cl- channels. In contrast, UK-5099, DISA, and MK-473 were nonspecific in that the compounds displayed comparable suppressive effects on all three parameters. Structure-activity relationships in the MK-447 series revealed the critical elements of the molecule responsible for drug potency. In particular, the importance of the neighboring ionizable 1-hydroxyl and 2-aminomethyl groups and the formation of secondary ring structures for biological activity is emphasized. The most potent derivative thus far identified, termed analogue A [inhibitor constant (Ki) approximately 16 microM], had a potency approximately sixfold greater than that of the parent compound (Ki approximately 90 microM). These findings define the mechanism of action of a relatively new class of agents that behave as inhibitors of swelling-activated Cl- channels in these cells.
Butylated Hydroxytoluene↗
Lactic acid secretion by human neutrophils. Evidence for an H+ + lactate- cotransport system.
The pathway by which L-lactate (Lac) crosses the plasma membrane of isolated human neutrophils was investigated. The influx of [14C]Lac from a 2 mM Lac, 145 mM Cl-, 5.6 mM glucose medium was approximately 1.5 meq/liter of cell water.min and was sensitive to the organomercurial agent mersalyl (apparent Ki approximately 20 microM), to alpha-cyano-4-hydroxycinnamate (CHC), the classical inhibitor of monocarboxylate transport in mitochondria, and to UK-5099 (apparent Ki approximately 40 microM), a more potent analogue of CHC. Transport was also strongly blocked (greater than 80%) by 1 mM of either 3,5-diiodosalicylic acid, MK-473 (an indanyloxyacetate derivative), or diphenyl-amine-2-carboxylate, and by 0.4 mM pentachlorophenol, but not by 1 mM ethacrynic acid, furosemide, or the disulfonic stilbenes SITS or H2DIDS. One-way [14C]Lac efflux from steady-state cells amounted to approximately 6 meq/liter.min and was likewise affected by the agents listed above. Influx, which was membrane potential insensitive and Na+ independent, displayed a strong pH dependence: extracellular acidification enhanced uptake while alkalinization inhibited the process (pK' approximately 5.7 at 2 mM external Lac). The rate of [14C]Lac influx was a saturable function of external Lac, the Km being approximately 7 mM. Steady-state cells exhibited an intracellular Lac content of approximately 5 mM and secreted lactic acid into the bathing medium a a rate of approximately 4 meq/liter.min. Secretion was completely suppressed by 1 mM mersalyl which inactivates the carrier, leading to an internal accumulation of Lac. That the Lac carrier truly mediates an H+ + Lac- cotransport (or formally equivalent Lac-/OH- exchange) was documented by pH-stat techniques wherein an alkalinization of poorly buffered medium could be detected upon the addition of Lac; these pH changes were sensitive to mersalyl. Thus, the Lac carrier of neutrophils possesses several features in common with other monocarboxylate transport systems in erythrocytes and epithelia.
Biological Transport↗
Use of tributyltin to probe contribution of Cl(-)-HCO3- exchange to regulation of steady-state pHi in human neutrophils.
Organotin derivatives represent a class of artificial ionophores that mediate Cl(-)-OH- exchange and thereby facilitate the chemical equilibrium distribution of Cl- and H+ across biological membranes. Imposing different pH and Cl- gradients by varying extracellular pH (pHo) and extracellular [Cl-] in the presence of 1 microM tributyltin validated the above assumptions in human neutrophils. Under relatively alkaline conditions [intracellular pH (pHi) greater than or equal to 7.10 and pHo greater than or equal to 7.40], the cell's natural Cl(-)HCO3- exchanger mimicked the actions of the tributyltin compound and was the principal factor controlling steady-state pHi. However, with increasing extracellular acidification, there was a progressive deviation from the predicted equilibrium distribution in the case of the normal Cl(-)-HCO3- transport system, whereas tributyltin-treated cells followed theoretical expectations. Exposure of neutrophils to a number of inhibitors of Cl(-)-HCO3- exchange led to a fall in pHi, apparently confirming the impression that a net HCO3- influx through Cl(-)-HCO3- countertransport was chiefly responsible for maintaining steady-state pHi. However, this intracellular acidification could be satisfactorily ascribed to proton movements through a parallel pathway, namely nonionic diffusion of the free acid form of the drugs. These results imply that Cl(-)-HCO3- exchange is the dominant pH regulatory device only under relatively alkaline conditions and that other mechanisms in addition to Na(+)-H+ exchange are likely to play an important role in recovery from acidification and in maintaining steady-state pHi. The possibility that the lactate carrier may function in this capacity is discussed.
Carrier Proteins↗
Cilastatin does not alter superoxide dismutase activity.
Cilastatin inhibits dehydropeptidase-I, a zinc metaloenzyme that metabolizes imipenem. Because zinc stabilizes the mammalian superoxide dismutase, we postulated that cilastatin would also inhibit the dismutase. Cilastatin concentrations at levels threefold higher than those expected in urine, however, did not inhibit the superoxide dismutase activity.
Cilastatin↗
Role of fibronectin in human monocyte and macrophage bactericidal activity.
Fibronectin is a high-molecular-weight glycoprotein found as a soluble dimer in plasma and as an insoluble multimer in tissues. It has been proposed that plasma fibronectin facilitates phagocytic removal of lysed cells and damaged tissues. Fibronectin binds avidly to several species of gram-positive bacteria and enhances staphylococcal and streptococcal attachment to cultured cells. Determination of whether fibronectin will enhance the bactericidal activity of monocytes and macrophages has not been reported. The bactericidal activity of freshly isolated monocytes, cultured monocytes, or lymphokine-activated macrophages was tested in the presence of either dimeric or multimeric fibronectin. Freshly isolated monocytes and lymphokine-activated macrophages killed Staphylococcus aureus effectively in the absence of fibronectin or whole serum. In contrast, monocytes cultured for 7 to 10 days had diminished staphylocidal capacity. When the monocytes were cultured with either dimeric or multimeric fibronectin, however, bactericidal capacity was maintained. Thus, although fibronectin did not enhance the bactericidal activity of mononuclear phagocytes, both multimeric and dimeric fibronectin were effective at maintaining the bactericidal capacity.
Blood Bactericidal Activity↗
Activation and inhibition of Limulus amebocyte lysate coagulation by chemically defined substructures of lipid A.
Recent work with lipid mutants of Escherichia coli and Salmonella typhimurium has helped to elucidate the correct structure of lipid A and has suggested a biosynthetic pathway. Precursor molecules include diacylglucosamine 1-phosphates and tetraacyl disaccharide bis-phosphates. The activities of several of these compounds and of their derivatives were measured by Limulus amebocyte lysate (LAL) assay. We report that (i) both mono- and disaccharide precursors of lipid A activate LAL, (ii) two acyl chains on the monosaccharide subunit of lipid A are necessary for activation of LAL, and (iii) the monosaccharide, 2-monoacylglucosamine 1-phosphate can competitively inhibit LAL activation by diacyl monosaccharide lipid A precursors. However, 2-monoacylglucosamine 1-phosphate did not inhibit endotoxin activation of LAL. One unanticipated finding was that the activities of the monosaccharides were reduced upon storage even though their covalent structures were unchanged. Perhaps this is due to alterations in physical state. Thus, these lipid A precursors and derivatives offer some insight into the structural features required for activation of the LAL assay and may in the future provide derivatives which are competitive inhibitors of endotoxin.
Drug Stability↗
Effects of subinhibitory concentrations of antibiotics on Staphylococcus aureus interactions with fibronectin.
Bacterial adherence to host tissues relies on interactions between tissue macromolecules and bacterial surface molecules. One of the major predisposing factors to infection with Staphylococcus aureus is trauma to tissues. A common element in traumatized tissues is fibronectin. In previous studies, we have shown that fibronectin binds to Staph. aureus. In this paper, we have investigated the effects of subinhibitory concentrations of antibiotics on fibronectin interactions with Staph. aureus. Exposure of Staph. aureus to 1/4 MIC of penicillin increases the number of binding sites and enhances adherence of Staph. aureus to a collagen-fibronectin matrix. Chloramphenicol, erythromycin, clindamycin, and U57,930E all decreased the number of binding sites. Also, U57,930E reduced Staph. aureus adherence to a collagen-fibronectin matrix. Taken together, these data suggest that penicillin may enhance Staph. aureus adherence to tissue fibronectin whereas U57,930E might reduce such binding.
Anti-Bacterial Agents↗