Publications by authors named "Jung A Han"

In contrast to the conventional belief that systemic arteries dilate under hypoxia, we found that α-adrenergic contraction of rat deep femoral artery (DFA) is largely augmented by hypoxia (HVC(DFA)) while hypoxia (3% Po(2)) alone had no effect. HVC(DFA) was consistently observed in both endothelium-intact and -denuded vessels with partial pretone by phenylephrine (PhE) or by other conditions (e.g.

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Hypoxia-induced pulmonary vasoconstriction (HPV) is critical for matching of ventilation/perfusion in lungs. Although hypoxic inhibition of K(+) channels has been a leading hypothesis for depolarization of pulmonary arterial smooth muscle cells (PASMCs) under hypoxia, pharmacological inhibition of K(+) channels does not induce significant contraction in rat pulmonary arteries. Because a partial contraction by thromboxane A(2) (TXA(2)) is required for induction of HPV, we hypothesize that TXA(2) receptor (TP) stimulation might activate depolarizing nonselective cation channels (NSCs).

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The objective of this study was to identify some proteins associated with testosterone-related differences in myogenesis and adipogenesis between bulls and steers. Global proteins were monitored in skeletal muscle and adipose tissue from bulls (n = 20) and steers (n = 20), respectively. We identified four differentially expressed (twofold or more) proteins in skeletal muscle from bulls, myosin light chain 1 (MLC1), ankyrin repeat domain-containing protein 1 (ANKRD1) and heat shock protein beta 1 (HSPB1) that were up-regulated and cofilin 2 (CFL2) that was down-regulated, and also identified two down-regulated proteins in adipose tissue, transaldolase 1 (TALDO1) and L: -lactate dehydrogenase B chain (LDHB).

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The objective of this study was to identify the proteins involved in bovine intramuscular fat (IMF) development. Global proteins were monitored in bovine skeletal muscle at muscle-developing versus IMF-increasing stages and with higher versus lower IMF scores, respectively. We identified two differentially expressed (two-fold or more) proteins at the IMF-increasing stage, up-regulated heat shock protein beta 1 (HSPB1) and down-regulated ATP synthase D chain (ATP5H), and two down-regulated proteins with higher IMF scores, carbonic anhydrase 2 (CA2) and myosin light chain 3 (MYL3).

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Nicotinamide at millimolar concentrations affects cell survival in various conditions, and is being utilized therapeutically in many human diseases. However, the effect of an acute treatment of nicotinamide at such high dose on gene expression and cellular metabolism has rarely been determined previously. In this study, we found that levels of O-N-acetylglucosamin(O-GlcNAc)ylated proteins including Sp1 acutely decreased upon treatment of 10 mM nicotinamide.

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Glaucoma and ocular hypertension are highly prevalent conditions in individuals over the age of 40 and are commonly seen together in patients with cardiovascular disease. Many of the antiglaucoma medications, when systemically absorbed, affect the sympathetic and parasympathetic nervous systems of patients and can cause cardiovascular toxicity. Such adverse effects are frequently associated with the long-term use of potentially toxic agents in elderly people, who are most prone to chronic eye disease.

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We found that the protein level of Sp1 transcription factor decreases as normal human fibroblasts undergo replicative aging. Sp1 also undergoes a rapid decrease in the protein level and activity in MCF-7 cells that are induced to a state of cellular senescence. In the cells treated with other DNA damaging chemicals such as actinomycin D and H(2)O(2), the Sp1 level decreased progressively as well.

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Replicative senescence limits the proliferation of somatic cells passaged in culture and may reflect cellular aging in vivo. The most widely used biomarker for senescent and aging cells is senescence-associated beta-galactosidase (SA-beta-gal), which is defined as beta-galactosidase activity detectable at pH 6.0 in senescent cells, but the origin of SA-beta-gal and its cellular roles in senescence are not known.

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