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Biomedical subjects

S Wessler

Publications and source records attributed to S Wessler.

At least 19 recordsLinked to original sources
PubMed1992

The splicing of transposable elements and its role in intron evolution.

Recent studies have demonstrated that transposable elements in maize and Drosophila are spliced from pre-mRNA. These transposable element introns represent the first examples of recent addition of introns into nuclear genes. The eight reported examples of transposable element splicing include members of the maize Ac/Ds and Spm/dSpm and the Drosophila P and 412 element families. The details of the splicing of these transposable elements and their relevance to models of intron origin are discussed.

Animals↗
PubMed1992

Estrogen-associated thromboembolism.

Most of the linkage of atherosclerosis and thrombosis with estrogens is epidemiologic in origin. Although the effects of estrogens on the mechanisms of hemostasis are wide ranging, many are benign; only a few may account for thrombus formation. Platelet function tests have provided extensive but contradictory data, and interpretation is limited because it is uncertain whether a rise in one or more of these parameters is a primary or secondary effect. The most consistent effects of estrogens on coagulation proteins are elevations of fibrinogen; factors II, VII, IX, X, and XII; protein C; and plasminogen. Although these elevations have been attributed to the estrogenic component in oral contraceptives, the progestogen concentration may also influence these increases. Among other coagulation proteins studied, the following are unaffected by oral contraceptive use: factors V, VIII, and XI; prekallikrein; and high-molecular-weight kininogen. In contrast, protein S values are decreased. The plasma concentration of plasmin inhibitor is unchanged, whereas both proteinase inhibitor and macroglobulin are significantly increased by oral contraceptive use. Cl esterase inhibitor is decreased in women taking oral contraceptives and correlates with the increase in Hageman factor. Antithrombin III is one plasma inhibitor for which a decrease in quantity and activity have been associated with a thrombotic tendency in humans. Although data on estrogen-associated changes in the quantity of antithrombin III have been conflicting, the ability of plasma to inhibit factor Xa is significantly reduced in a dose-dependent manner among pre- and postmenopausal estrogen users.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

Molecular analysis of the maize wx-B3 allele indicates that precise excision of the transposable Ac element is rare.

The somatic and germinal behavior of the maize wx-B3 mutation indicates that this Ac allele rarely reverts. Endosperms containing wx-B3 display tiny and infrequent Wx revertant sectors while no significant reversion is detected when wx-B3 pollen is stained with I/KI. Previous studies of other transposable element alleles that revert infrequently have implicated low levels of element excision. Unlike these other alleles, the wx-B3 Ac element is indistinguishable from fully active Ac elements with respect to its structure, and its ability to transpose from the Wx gene or to trans-activate a Ds element. Characterization of somatic and germinal excision events lead us to conclude that excision of the wx-B3 Ac element almost always produces null alleles. Furthermore, the excellent correlation between the position of the wx-B3 mutation on the physical and genetic maps indicates that the Ac insertion is the only lesion of wx-B3. As a result, precise excision of this Ac should restore Wx function. The fact that revertant sectors and pollen grains are rare indicates that precise excision of Ac is also rare. The finding that the wx-B3 reversion frequency is comparable whether wx-B3 is hemizygous or over a wx allele with a wild-type insertion site illustrates a fundamental difference between the excision mechanisms of Ac and Drosophila P elements.

Alleles↗
PubMed1990

Filler DNA is associated with spontaneous deletions in maize.

We have determined the structure of five spontaneous deletions within the maize waxy (Wx) gene. Of these, four were found in spontaneous wx mutants (wx-B, wx-B1, wx-B6, wx-C4) and include exon sequences; the fifth is restricted to an intron and represents a restriction fragment length polymorphism of a nonmutant allele (Wx-W23). The deletions, which range in size from 60 to 980 base pairs (bp), cluster in a G+C-rich region of approximately 1000 bp that is capable of forming stable secondary structures. Most striking is our finding that all of the alleles have DNA insertions (filler DNA) of 1-131 bp between the deletion endpoints. For three of the five deletions, the filler DNA and sequences at the deletion termini appear to be derived from sequences near one deletion endpoint. A previously reported spontaneous deletion of the maize bronze gene (bz-R) also contains filler DNA. The association of filler DNA with maize deletion endpoints contrasts dramatically with the rarity of similar events in animal germ-line and bacterial mutations.

Base Sequence↗
PubMed1987

Inactivation of the maize transposable element Activator (Ac) is associated with its DNA modification.

The Activator (Ac) element at the waxy locus (wx-m7 allele) has the ability to undergo changes in its genetic activity and cycles between an active and inactive phase. Comparison of active Ac elements at several loci and the inactive Ac at wx-m7 by Southern blot analysis revealed that the inactive Ac sequence was not susceptible to digestion by the methylation sensitive enzyme PvuII while active elements were susceptible to PvuII digestion. Restriction digest comparisons between the clones of the active and inactive Ac elements were indistinguishable. Further analyses with the enzymes SstII and the methylation sensitive and insensitive isoschizomers EcoRII and BstNI showed the inactive Ac sequence was methylated at these sites, whereas the active Ac was hypomethylated. Although the active Ac at the wx-m7 allele in different genetic backgrounds showed differences in the Ac DNA modification pattern, at least a fraction of genomic DNA contained Ac sequences that were unmethylated at all of the internal sites we assayed. These data may suggest a role for DNA modification in the ability of Ac to transpose from the waxy locus and to destabilize unlinked Ds elements.

Alleles↗
PubMed1987

Anticoagulants in the prevention of embolic stroke. Part I.

Cardiac lesions among those at high risk of cerebral emboli include: atrial fibrillation, rheumatic mitral valve disease, acute myocardial infarction, prosthetic heart valves, and idiopathic dilated cardiomyopathy. Many of these patients can be protected from cerebral infarction by anticoagulants. Following a cardiac embolic stroke, CT scans are critical in deciding for whom and at what time anticoagulation should be considered. From studies of CT and cerebrovascular pathology, it has become clear that it is the cerebral infarct rather than the arterial occlusion that provides the key piece of information in deciding whether and when anticoagulants should be considered for the secondary prevention of cardiac emboli among patients who present with a clinical stroke.

Aged↗
PubMed1987

Antiheparin antibodies: their preparation and use in a heparin immunoassay.

Antibodies that recognize unmodified heparin bound to positively charged macromolecules have been obtained by immunizing rabbits with a methylated bovine serum albumin-heparin precipitate. These antibodies have been used to develop an immunoassay that can quantitate heparin at a concentration of 5 ng/ml in buffer solutions, and at a concentration of 25 ng/ml in plasma without pretreatment of the sample. The specificity of the antibodies is such that they do not recognize other glycosaminoglycans and are able to distinguish among different commercial heparin samples that are otherwise indistinguishable by specific anticoagulant activity or molecular weight distribution.

Animals↗
PubMed1987

What's the dose?

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Humans↗
PubMed1987

Prophylactic anticoagulants in managing embolic stroke.

The primary risk of anticoagulant therapy in cardiac embolic stroke is hemorrhage--particularly cerebral hemorrhage in the elderly. Improving the benefit/risk ratio for indicated anticoagulation involves consideration of the following: hemostatic competence, blood pressure, drug interactions, falls, interval surgery, diet, aspirin and last but not least, the intensity of anticoagulant prophylaxis. For the present it would be prudent to limit heparin administration to a low-dose regimen not exceeding 20,000 units/24 hours and warfarin maintenance to a low-dose prothrombin time ratio of 1.5.

Accidental Falls↗
PubMed1986

Pharmacology of heparin and warfarin.

Thromboembolic obstruction to three major components of the circulation--arterial, venous and intravascular foreign surfaces--contributes to premature death and disability in Western society. In many, but not all, of these conditions associated with thromboembolism, heparin and warfarin are the drugs of choice. It is the purpose of this presentation to provide some common ground in the area of anticoagulant prophylaxis that will be of intrinsic value for decision making in cardiac, cerebral and peripheral vascular disease. Only those aspects of the hemostatic mechanism most relevant to the antithrombotic action of heparin and warfarin are discussed. Assays for both drugs as well as some practical guidelines for their use in low, medium and high dose regimens are outlined. Techniques for improving the benefit/risk ratio for each drug are specifically detailed.

Antithrombin III↗
PubMed1985

Preparation and identification of a population of antibodies that recognize carbodiimide-modified heparin.

Protein-heparin complexes, prepared by a water-soluble carbodiimide coupling technique, were used to produce anti-heparin antibodies in rabbits. Antiserums that recognized carbodiimide-treated heparin, but not untreated heparin, were obtained. Carbodiimide-treated heparan sulfate exhibited 10% to 20% cross-reactivity compared with a similarly treated heparin, whereas there was no cross-reactivity with five other carbodiimide-treated mucopolysaccharides. 3H-1-ethyl-3-(3-trimethylammoniumpropyl) carbodiimide iodide was used to demonstrate that carbodiimide forms a stable adduct with heparin and other mucopolysaccharides. Using an antibody fraction that eluted from 1-ethyl-3-(3-trimethylammoniumpropyl) carbodiimide iodide-treated heparin-Sepharose with 2 mol/L KI, it was demonstrated that, for the antibody population studied, the addition of one carbodiimide per heparin molecule resulted in complete epitope expression without loss of anticoagulant activity. The addition of up to eight additional carbodiimide molecules to heparin did not increase the extent of epitope formation, although anticoagulant activity was lost. Except for heparan sulfate, the addition of radiolabeled carbodiimide to other mucopolysaccharides did not result in epitope formation. These data demonstrate that antibodies to an epitope derived from heparin can be formed, that the epitope is fully expressed while anticoagulant activity is present, and that the antibody is specifically directed against an altered portion of the polysaccharide.

Animals↗