Marilyn Mielke

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The SIR1 gene is one of four specialized genes in Saccharomyces cerevisiae required for repressing transcription at the silent mating-type cassettes, HMLalpha and HMRa, by a mechanism known as silencing. Silencing requires the assembly of a specialized chromatin structure analogous to heterochromatin. FKH1 was isolated as a gene that, when expressed in(More)
A hallmark of neurodegenerative diseases caused by polyglutamine expansion is the abnormal accumulation of mutant proteins into ubiquitin-positive inclusions. The local build-up of these ubiquitinated proteins suggests that the proteasome machinery inadequately clears misfolded proteins, resulting in their increase to potentially toxic levels. Inclusions(More)
Undifferentiated oligoarthritis (UOA) resembles clinically reactive arthritis (ReA), but does not fulfill the diagnostic criteria. In 46 patients with UOA, in 16 with ReA, and in 15 with rheumatoid arthritis (RA) the humoral and cellular immune response to the ReA-associated bacteria Chlamydia trachomatis, Yersinia enterocolitica, Shigella flexneri,(More)
Efficient labeling of short oligos at their 3'-ends was achieved through polymerase chain reaction. The length of cycled-labeled oligos can be accurately predicted by omitting one or more dNTPs in the labeling step. Thus, labeled oligos can be simply column-purified, eliminating the need for tedious gel purification. We demonstrated the effectiveness of(More)
A number of investigations have noted that functional biological assays for heparin are not always reliable and may not reflect the actual biochemical level of heparin in patients receiving anticoagulant therapy. This creates the possibility that patients receiving anticoagulant treatment may have an excess or deficiency of circulating levels of heparin. To(More)
Activation of the Na(+)/H(+) exchanger may play an important role in the development of cardiac hypertrophy. Isolated ventricular myocyte studies have suggested that angiotensin II (AII) has direct positive inotropic effect caused by intracellular alkalinization due to increased Na(+)/H(+) exchange, but whether this occurs in the whole heart is unknown.(More)
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