Byung Gu Yoon

Cognitive impairment is significantly associated with lower BMD in postmenopausal women. This finding suggests that cognitive aging is clearly multifactorial, but estrogen deficiency may be one of the contributing factors.

OBJECTIVE: The aim of the study was to explore the therapeutic potential of menopausal hormone therapy (MHT) in women with mild cognitive impairment (MCI). METHODS: Thirty-seven postmenopausal women (age range: 57-82 y) with multiple-domain, amnestic subtype MCI were randomly assigned to either placebo (n = 18) or MHT (n = 19) for 24 months (percutaneous estradiol [E2] gel [0.1%, 2 mg/d] and oral micronized progesterone [MP4] [100 mg/d]). All participants received donepezil, and apolipoprotein E

17Beta-E2 inhibits in vitro VSMC proliferation induced by lysoPC via a nongenomic antioxidant mechanism.

BACKGROUND: Estrogen therapy in early menopausal women decreases the risk of coronary heart disease and parenteral, but not oral, estrogen is reported to reduce blood pressure (BP). Progestogens are typically added to estrogens to prevent unopposed endometrial stimulation. The effects of progestogen on BP have been less well studied to date. This study was conducted to explore the impacts of micronized progesterone (MP4) combined with percutaneous estradiol gel (PEG) on hemodynamics in postmenop

The balance between tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) regulates fibrinolysis. PAI-1 expression increases in atherosclerotic arteries and vascular smooth muscle cells (VSMCs) are one of major constituents of atheroma. We investigated the impact of lysophosphatidylcholine (lysoPC), an active component of oxidized low-density lipoprotein, on the plasminogen activator system of the rat VSMCs. The lysoPC stimulated the protein and gene express

MHT might not differ from risedronate in the prevention of secondary fractures and death among postmenopausal women with recent hip fracture.

The balance between tissue-type plasminogen activator (t-PA) and plasminogen activator inhibitor type 1 (PAI-1) regulates fibrinolysis. PAI-1 expression increases in atherosclerotic arteries and vascular smooth muscle cells (VSMCs) are one of major constituents of atheroma. We investigated the impact of lysophosphatidylcholine (lysoPC), an active component of oxidized low-density lipoprotein, on the plasminogen activator system of the rat VSMCs. The lysoPC stimulated the protein and gene express

This study evaluated the effects of combination treatment with alendronate (ALEN) and hormone therapy (HT) on bone mineral density (BMD) in postmenopausal Korean women. This multicenter, randomized, controlled clinical trial enrolled 344 postmenopausal women with low BMD. The women received HT (0.625 mg/day of conjugated equine estrogen and 2.5 mg/day of medroxyprogesterone acetate) alone or in combination with ALEN (10 mg/day) for 1 year. Changes in BMD and biochemical markers of bone turnover

Compared with HT alone, the addition of ALEN to ongoing HT for 1 year does not make a difference in BMD among postmenopausal Korean women with low BMD.

In cultured VSMCs treated with lysoPC, 17β-E₂ reduced apoptotic cell death by down-regulating both extrinsic and intrinsic apoptosis pathways, contributing to the preventive action of MHT against CHD.

In VSMCs stimulated with lysoPC, 17β-E₂ reduced PAI-1 expression through a non-receptor-mediated mechanism via antioxidant activity as well as a receptor-mediated mechanism; however, it did not alter t-PA secretion. Of note, 17β-E₂ suppressed PAI-1 activity and concurrently enhanced t-PA activity, suggesting a beneficial influence on fibrinolysis.

This study evaluated the effects of combination treatment with alendronate (ALEN) and hormone therapy (HT) on bone mineral density (BMD) in postmenopausal Korean women. This multicenter, randomized, controlled clinical trial enrolled 344 postmenopausal women with low BMD. The women received HT (0.625 mg/day of conjugated equine estrogen and 2.5 mg/day of medroxyprogesterone acetate) alone or in combination with ALEN (10 mg/day) for 1 year. Changes in BMD and biochemical markers of bone turnover