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Biomedical subjects

D J Weiss

Publications and source records attributed to D J Weiss.

At least 109 records · Page 6Linked to original sources
PubMed1990

Surface-activated bovine platelets do not spread, they unfold.

The present study has examined the response of bovine platelets to surface activation and compared it to the reaction of human cells. Human platelets react to surfaces by losing their discoid shape, extending pseudopods, converting to dendritic forms, and finally, spreading into thin films resembling pancakes. Bovine platelets do not spread, they unfold. Surface activation causes them to transform from discs to irregular, flattened shapes resembling dendritic platelets, but they are unable to fill in spaces between pseudopods, a step required for spreading. Bovine platelets lack the surface-connected open canalicular system (OCS), which serves as a reservoir of membrane for human platelet spreading. Its absence may be the major factor in the failure of bovine platelet spreading, but there are other possible factors. Circumferential microtubules are more resistant to disassembly in surface-activated bovine than human cells, and their stability as rings or fractured bundles may limit spreading. Actin filament assembly is similar in human and bovine platelets, but the organization is different. Human platelets form a peripheral weave of actin that expands the membrane between pseudopods. A peripheral weave does not form in surface-activated bovine platelets. The absence of the OCS and differences in cytoskeletal organization in bovine platelets may also affect spreading of the surface membrane. Fibrinogen-gold (Fgn-Au) probes added to spread human platelet move from pseudopods and the cell margin toward the center and concentrate in the OCS. Fgn-Au particles bind to surface-activated bovine cells, but move very little, or not at all. All of these factors may contribute to the inability of bovine platelets to react to surfaces by spreading like human cells, but absence of the OCS appears to be the major cause.

Animals↗
PubMed1989

Isolation of granulocytes and mononuclear cells from the blood of dogs, cats, horses and cattle.

A simple discontinuous Percoll density-gradient technique was adapted for isolation of granulocytes and mononuclear cells from cats, dogs, horses and cattle. Separation was accomplished at low speeds using a standard tabletop centrifuge. Cell purity was 100% for both granulocytes and mononuclear cells and cell viability exceeded 95%. Percent recovery of leukocytes ranged from 69 to 83%.

Journal Article↗
PubMed1989

Idiopathic dyserythropoiesis in a dog.

Idiopathic dyserythropoiesis in a dog was characterized by chronic nonregenerative normocytic normochromic anemia, cellular marrow and abnormal morphology of erythroid precursors. Serum concentrations of Vitamin B(12), folate and iron were inconsistent with secondary causes of dyserythropoiesis. The disorder appeared to be distinct from myelodysplastic syndromes described previously.

Journal Article↗
PubMed1989

Comparison of bovine and human platelet deformability, using micropipette elastimetry.

We evaluated the deformability of bovine platelets and contrasted the effects of pharmacologic and thermal perturbations on cytoskeletal structure of human and bovine platelets. Platelets were aspirated into micropipettes (0.7 to 0.8 micron in diameter) by stepwise increments in tension. The resulting lengths of the cell extensions were recorded. The cell extensions aspirated from bovine platelets were shorter than the extensions drawn from human platelets. Disassembly of the circumferential microtubule coil allowed human platelets to pass through the pipette, but the same treatments only slightly increased the deformability of bovine platelets. Alteration of the actin filament cytoskeleton caused increased mechanical fragility of human platelets. In contrast, even the combined use of microtubule and actin filament-disrupting agents only modestly increased the deformability of bovine platelets and did not cause premature fragmentation of the cells. Unusual cytoskeletal structure, absence of an open canalicular system, and disparity in granule size may all contribute to the variance in deformability between the platelets of the 2 species. Reduced cell deformability may impair bovine platelet surface interactions by diminishing the ease of cell spreading and formation of areas of contact between the platelet and other cell surfaces.

Actin Cytoskeleton↗
PubMed1988

Non-genomic effects of estrogens and antiestrogens.

In addition to the effects of estrogens on transcription, mediated by the estrogen receptor, and the antiestrogenic effects of triphenylethylene derivatives resulting from their competitive action at the estrogen receptor level, estrogens and antiestrogens can affect cellular processes though other mechanisms. Estrogens can bind and alter enzymatic activities in membranes isolated from target cells, can influence the activities of purified enzymes and can change cell permeability and polarization under conditions excluding transcriptional effects. Triphenylethylene antiestrogens at micromolar concentrations can affect cholinergic, histaminergic and dopaminergic systems, affect calmodulin action and influence protein kinase C activity. Tamoxifen added to suspension of human endometrial adenocarcinoma cells at concentrations greater than 10 microM both increased phosphoinositide hydrolysis and inhibited the stimulatory effect of carbachol on this system. These effects, however, may represent nonspecific actions of the antiestrogens, shared with the structurally related phenothiazines, on the plasma membrane.

Animals↗
PubMed1988

Susceptibility of canine, feline and human erythrocytes to oxidant-mediated injury.

e relative susceptibilities of feline, canine and human erythrocytes to in vitro hydrogen peroxide-induced lipid peroxidation and hemolysis were studied. At 15 minutes following exposure to hydrogen peroxide, cat erythrocytes had higher concentrations of lipid peroxidation by-products and a greater percent hemolysis as compared to dogs and humans. Erythrocytes from cats with induced sterile abscesses had lower concentrations of the antioxidant glutathione, but they did not have detectable concentrations of lipid peroxides nor were they more susceptible to in vitro lipid peroxidation or hemolysis.

Journal Article↗
PubMed1988

Studies on the pathogenesis of the erythrocyte destruction associated with the anemia of inflammatory disease.

Density-separated feline RBC were analyzed for surface immunoglobulin and in vitro susceptibility to macrophage phagocytosis before and after introduction of a sterile abscess. Prior to abscess induction, least dense cells did not have detectable surface immunoglobulin G (IgG) as a direct antiglobulin reaction was negative. Two of four intermediate and three of four most dense cell fractions had detectable surface IgG as indicated by a positive direct antiglobulin reaction. On Days 3 and 5 after induction of sterile abscesses all three RBC fractions were positive and the size of the RBC clumps tended to increase. In vitro macrophage phagocytosis of all three RBC fractions increased significantly after abscess induction. The phagocytosis could be partially blocked by preincubation of macrophages with feline IgG.

Journal Article↗
PubMed1988

Neutrophil-induced erythrocyte injury: a potential cause of erythrocyte destruction in the anemia associated with inflammatory disease.

Activated neutrophils at effector/target ratios of 1:20 to 1:2,000 induced depletion of red blood cell (RBC)-reduced glutathione, increased membrane-bound hemoglobin and methemoglobin, and promoted immunoglobulin binding to the cell membrane. Superoxide dismutase/catalase ameliorated the decrease in reduced glutathione and the increase in methemoglobin and immunoglobulin binding. This is interpreted as evidence that activated neutrophils can alter the antigenic nature of the RBC membrane through generation of toxic oxygen radicals.

Anemia, Hemolytic↗
PubMed1988

Regulation of phosphoinositide hydrolysis in transformed human endometrial cells.

Addition of the cholinergic agents acetylcholine or carbamylcholine (CCh) to suspensions of human endometrial adenocarcinoma cells (Ishikawa line) preincubated with [3H] myoinositol promoted a rapid concentration-dependent hydrolysis of labeled phosphoinositides to inositol tris-, bis-, and monophosphates with EC50 values (mean +/- SE) of 3.5 +/- 1.6 and 26.5 +/- 4.8 microM, respectively. Atropine inhibition of the CCh effects (Ki = 1.6 +/- 1.3 nM) and the ineffectiveness of nicotinic antagonists indicate involvement of a muscarinic receptor. Both basal and CCh-stimulated production of inositol phosphates were higher in the presence of LiCl. The effect of LiCl on inositol monophosphate accumulation was concentration dependent (1-100 mM). Vasopressin, oxytocin, phenylephrine, histamine, and prostaglandin F2 alpha, had no apparent affect on inositol phosphate levels. Phorbol esters inhibited up to 35% of the effect of CCh on inositol phosphate accumulation. Triphenylethylene antiestrogens at micromolar concentrations increased inositol phosphate accumulation, but inhibited the effects of CCh. However, the rapid uptake of trypan blue observed after exposure to 10 microM tamoxifen suggests an alteration of the plasma membrane which may affect signal-transducing systems. The effects of CCh on the production of inositol phosphates and the expected concomitant liberation of diacylglycerol by transformed epithelial cells of human endometrium are of potential significance in normal endometrial physiology, since cholinergic innervation of endometrial glands has been reported, and the role of hormonally stimulated phosphoinositide hydrolysis in secretory mechanisms has been demonstrated in many systems.

Acetylcholine↗
PubMed1987

Aplastic anemia associated with trimethoprim-sulfadiazine and fenbendazole administration in a dog.

A dog that was treated with trimethoprim-sulfadiazine and fenbendazole developed transient aplastic anemia. The onset of bone marrow aplasia at 14 days after initiation of treatment and remission of it after cessation of treatment suggested that the aplasia was drug-induced. A hematologically normal dog treated with the same drug combination failed to develop hematologic dyscrasia. Because of the potential toxic effects of trimethoprim-sulfadiazine and/or fenbendazole, animals under treatment with this combination should be monitored by use of periodic CBC.

Anemia, Aplastic↗
PubMed1986

Potential role of serum inhibitors of erythropoiesis in the anemia associated with infection, renal disease and malignancy in the dog.

Serum from dogs with anemia secondary to infection, malignancy and chronic renal disease was tested for the capacity to inhibit in vitro erythropoiesis. Serum inhibition was found in seven of 10 dogs with infectious diseases, four of 10 dogs with malignant diseases, and two of 10 dogs with chronic renal failure. The results were reproducible with at least three different marrow donor dogs. Serum inhibition did not correlate with decreased packed cell volumes. However, serum inhibition occurred in the two dogs with greatest azotemia suggesting that inhibitors of erythropoiesis are present only in advanced stages of renal failure.

Journal Article↗
PubMed1986

Antibody-mediated suppression of erythropoiesis in dogs with red blood cell aplasia.

Eight dogs with acquired RBC aplasia were studied. Unfractionated sera and serum immunoglobulin G fractions were examined for the presence of erythroid progenitor cell inhibitors. A serum immunoglobulin G inhibitor directed against precursors of erythroid colony-forming units was detected in 3 of 5 dogs that were direct Coombs' test-negative and in 1 of 3 dogs that were direct Coombs' test-positive. Sera from these dogs were treated with binary ethyleneimine to inactivate any viruses present. The inhibitory effects of the treated serum on erythroid colony-forming units was not ameliorated.

Animals↗
PubMed1985

Myelodysplastic syndrome in two dogs.

Two cases of myelodysplastic syndrome in the dog are described. Both cases were characterized by hepatomegaly, cytopenias, macrocytosis, cellular bone marrow, and dysplastic changes in all hematopoietic cell lines. Serum vitamin B12 and folic acid concentrations were within reference ranges in one dog, but vitamin B12 was slightly decreased in the other. Vitamin B12 therapy did not result in amelioration of the hematologic disorder. The duration of illness was approximately 5 months. Necropsy of one dog revealed an acute undifferentiated leukemia.

Anemia↗
PubMed1985

Secondary myelofibrosis in three dogs.

Myelofibrosis was diagnosed in 3 dogs. In each dog, there was evidence of concurrent bone marrow necrosis, suggesting that the myelofibrosis was a secondary change. This suggestion was supported by a lack of dysplastic changes in hematopoietic cells. Bone marrow necrosis in 2 of the dogs may have been the result of widespread malignancy. Reversal of the myelofibrosis in 1 dog suggested that myelofibrosis is not always a terminal disorder.

Adenocarcinoma↗
PubMed1985

Bone marrow necrosis in the dog.

Bone marrow necrosis in 4 dogs was characterized by refractory anemia with or without leukopenia and thrombocytopenia. Romanovsky-stained bone marrow had a diffuse blue discoloration, and marrow particles were elongated. Degenerating cells, cellular debris, and vacuolated macrophages also were seen. Examination of bone marrow sections revealed extensive replacement of normal stroma by necrotic debris and hemorrhage. The cause of the necrosis was not determined. Concomitant disorders included chronic ehrlichiosis, estrogen toxicosis, malignancy, endometrial cystic hyperplasia, and glomerulonephritis.

Anemia, Aplastic↗