Menopause is clinically diagnosed as a condition when a woman has not menstruated for one year. During the menopausal transition period, there is an emergence of various lipid metabolic disorders due to hormonal changes, such as decreased levels of estrogens and increased levels of circulating androgens; these may lead to the development of metabolic syndromes including cardiovascular diseases and type 2 diabetes. Dysregulation of lipid metabolism affects the body fat mass, fat-free mass, fatty acid metabolism, and various aspects of energy metabolism, such as basal metabolic ratio, adiposity, and obesity. Moreover, menopause is also associated with alterations in the levels of various lipids circulating in the blood, such as lipoproteins, apolipoproteins, low-density lipoproteins (LDLs), high-density lipoproteins (HDL) and triacylglycerol (TG). Alterations in lipid metabolism and excessive adipose tissue play a key role in the synthesis of excess fatty acids, adipocytokines, proinflammatory cytokines, and reactive oxygen species, which cause lipid peroxidation and result in the development of insulin resistance, abdominal adiposity, and dyslipidemia. This review discusses dietary recommendations and beneficial compounds, such as vitamin D, omega-3 fatty acids, antioxidants, phytochemicals—and their food sources—to aid the management of abnormal lipid metabolism in postmenopausal women.

Sclerostin decreases bone mass by antagonizing the Wnt signaling pathway. We examined whether obesity-induced bone loss is associated with the expression of sclerostin. Five-week-old male mice were assigned to one of two groups (n = 10 each) and fed either a control diet (10% kcal from fat; CON) or a high-fat diet (60% kcal from fat; HF) for 12 weeks. Thex final body weight and whole body fat mass of the HF mice were higher than those of the CON mice. The distal femur cancellous bone mineral density and bone formation rate was lower in HF mice than in CON mice. The percent erosion surface was higher in the HF mice than the CON mice. The serum levels and femoral osteocytic protein expression levels of tumor necrosis factor-α (TNF-α) were significantly higher in HF mice than in CON mice. Sclerostin mRNA levels and osteocytic sclerostin protein levels in femoral cortex were also higher in HF mice than in CON mice. Sclerostin expression in MLO-Y4 osteocytes increased with TNF-α treatment, and TNF-α-induced sclerostin expression was blocked by the inhibition of NF-κB activation. Chromatin immunoprecipitation and a luciferase reporter assay demonstrated that NF-κB directly binds to the NF-κB binding elements on the mouse sost promoter and stimulates sclerostin expression. These results support a model in which, in the context of obesity or other inflammatory diseases that increase the production of TNF-α, TNF-α upregulates the expression of sclerostin through NF-κB signaling pathway, thus contributing to bone loss.

Host immune response is known to contribute to the progression of periodontitis, and alveolar bone destruction in periodontitis is associated with enhanced osteoclast activity. Therefore, we evaluated the roles of activated lymphocyte subsets in osteoclastogenesis. Osteoclast precursors were co‐cultured with activated lymphocytes (B, CD4+ T, CD8+ T) in the presence of either macrophage colony‐stimulating factor (M‐CSF) alone or M‐CSF plus soluble receptor activator of NF‐κB ligand (sRANKL), and subsequent differentiation into active osteoclasts was evaluatedby a resorption assay. The activated B and CD4+ cells, but not CD8+ T cells, induced osteoclast differentiation in the presence of M‐CSF alone. In the presence of M‐CSF and sRANKL, B cells induced the formation of small but highly active osteoclasts and increased resorption, while CD8+ T cells profoundly suppressed osteoclastogenesis. Co‐culture using an insert wellor supernatant suggested that both B and CD8+ T cells acted on osteoclasts mostly via soluble proteins. Activated B cells expressed many osteoclastogenic factors including RANKL, TNF‐α, IL‐6, MIP‐1α, and MCP‐3. CD8+ T cells expressed a substantial amount of osteoprotegerin (OPG) along with RANKL. However, blocking antibody to OPG did not reverse the suppression by CD8+ T cells, suggesting that other factor(s) are involved. Taken together, activated B cells promoted osteoclastogenesis, while CD8+ T cells inhibited the osteoclast formation via direct interaction. The results imply the importance of lymphocyte subpopulations in the development of periodontitis.

Oxidative stress in humans is associated with damage to DNA, proteins, and biological membranes. Oxidative stress, which often arises as a result of an imbalance in the human antioxidant status, has been implicated in aging and a number of human diseases such as cancer, atherosclerosis, and rheumatoid arthritis. This study was performed to test the hypothesis that the consumption of fruit juices may improve antioxidant status in human plasma. Ten healthy men 25-26 years old were recruited for the study. After overnight fasting, study subjects were fed 150 mL of fruit juice, and blood was collected at 0, 30, 60, 90, and 120 minutes after consumption. After a 1-day wash-out period, subjects were fed with the next sample of fruit juice until all nine juices (pear, apple, orange, grape, peach, plum, kiwi, melon, and watermelon) had been evaluated. All juices were prepared from pure fruits ground in a home-style mixer. Dietary food records and anthropometric measurements were used to evaluate the nutritional status of subjects. The antioxidant activities of fruit juices were estimated by measuring antioxidant status in the plasma using dichlorofluorescein (DCF) fluorescence. Except for pear juice, eight kinds of juices exhibited potent antioxidant effects in human plasma. Within 30 minutes after consumption, orange, melon, grape, peach, plum, apple, and kiwi juices already effectively suppressed reactive oxygen species generation. This radical scavenging effect of fruit juices was maintained for up to 90 minutes post-consumption, but the relative DCF fluorescence had rebounded to near the initial levels at 2 hours post-consumption in most samples tested. Interestingly, however, grape juice continuously exerted persistent antioxidant activity until 2 hours after supplementation. These results suggest that the consumption of fruits or fruit juices may reduce damage from oxidative stress, and that this effect may be a consequence of the antioxidant activity of fruits in scavenging the reactive oxygen species generated in human plasma. However, long-term studies with more subjects are needed to provide additional supportive evidence and better characterize the antioxidant properties of natural fruit juices.

We present a new, fast 3D traveltime calculation algorithm that employs existing frequency-domain waveequation downward-continuation software. By modifying such software to solve for a few complex (rather than real) frequencies, we are able to calculate not only the first arrival and the approximately most energetic traveltimes at each depth point but also their corresponding amplitudes. We compute traveltimes by either taking the logarithm of displacements obtained by the oneway wave equation at a frequency or calculating derivatives of displacements numerically. Amplitudes are estimated from absolute value of the displacement at a frequency. By using the one-way downgoing wave equation, we also circumvent generating traveltimes corresponding to near-surface upcoming head waves not often needed in migration. We compare the traveltimes computed by our algorithm with those obtained by picking the most energetic arrivals from finite-difference solutions of the one-way wave equation, and show that our traveltime calculation method yields traveltimes comparable to solutions of the one-way wave equation. We illustrate the accuracy of our traveltime algorithm by migrating the 2D IFP Marmousi and the 3D SEG/EAGE salt models.

Cyclooxygenase-2 (COX-2), an enzyme that catalyzes the synthesis of prostaglandins, is made inducible by various stimuli such as inflammation. Although COX-2 is commonly overexpressed in a variety of premalignant and malignant conditions including oral leukoplakia and squamous cell carcinoma, relatively little research has compared the effects of various COX-2 inhibitors (celecoxib, NS-398, nimesulide and meloxicam). Therefore, we investigated the effects of four different selective COX-2 inhibitors on the growth of KB cells, derived from oral squamous cell carcinoma (OSCC) and its mechanisms. Celecoxib and NS-398 strongly suppressed the proliferation of KB cells at 10-100 μM, whereas nimesulide and meloxicam are less potent proliferation inhibitors. Only celecoxib induced apoptosis of the KB cells, as detected on the basis of DNA fragmentation, caspase-3/7 activation and cleaved poly(ADP-ribose) polymerase (PARP) fragmentation. All four COX-2 inhibitors increased COX-2 protein expression but suppressed prostaglandin (PG) E 2 production in the KB cells, suggesting that the pro-apoptotic effect of celecoxib was unrelated to the inhibition of COX-2. Mechanistically, a high level of p53 protein and a low level of multidrug-resistant protein 1 (MRP1) and breast cancer resistant protein (BCRP) mRNA in KB cells with celecoxib may explain the differential effect of these selective COX-2 inhibitors in KB cells. Taken together, celecoxib is a good therapeutic candidate for treating OSCC through the suppression of cell proliferation and the induction of apoptosis in a COX-2 independent manner.

Because of its computational efficiency, prestack Kirchhoff depth migration remains the method of choice for all but the most complicated geological depth structures. Further improvement in computational speed and amplitude estimation will allow us to use such technology more routinely and generate better images. To this end, we developed a new, accurate, and economical algorithm to calculate first‐arrival traveltimes and amplitudes for an arbitrarily complex earth model. Our method is based on numerical solutions of the wave equation obtained by using well‐established finite‐difference or finite‐element modeling algorithms in the Laplace domain, where a damping term is naturally incorporated in the wave equation. We show that solving the strongly damped wave equation is equivalent to solving the eikonal and transport equations simultaneously at a fixed reference frequency, which properly accounts for caustics and other problems encountered in ray theory. Using our algorithm, we can easily calculate first‐arrival traveltimes for given models. We present numerical examples for 2‐D acoustic models having irregular topography and complex geological structure using a finite‐element modeling code.

Aging women experience hormonal changes, such as decreased estrogen and increased circulating androgen, due to natural or surgical menopause. These hormonal changes make postmenopausal women vulnerable to body composition changes, muscle loss, and abdominal obesity; with a sedentary lifestyle, these changes affect overall energy expenditure and basal metabolic rate. In addition, fat redistribution due to hormonal changes leads to changes in body shape. In particular, increased bone marrow-derived adipocytes due to estrogen loss contribute to increased visceral fat in postmenopausal women. Enhanced visceral fat lipolysis by adipose tissue lipoprotein lipase triggers the production of excessive free fatty acids, causing insulin resistance and metabolic diseases. Because genes involved in β-oxidation are downregulated by estradiol loss, excess free fatty acids produced by lipolysis of visceral fat cannot be used appropriately as an energy source through β-oxidation. Moreover, aged women show increased adipogenesis due to upregulated expression of genes related to fat accumulation. As a result, the catabolism of ATP production associated with β-oxidation decreases, and metabolism associated with lipid synthesis increases. This review describes the changes in energy metabolism and lipid metabolic abnormalities that are the background of weight gain in postmenopausal women.