Search

Abstract: The sol–gel process of producing SiO2–CaO bioactive glasses is well established, but problems remain with the poor mechanical properties of the amorphous form and the bioinertness of its crystalline counterpart. These properties may be improved by incorporating Na2O into bioactive glasses, which can result in the formation of a hard yet biodegradable crystalline phase from bioactive glasses when sintered. However, production of Na2O-containing bioactive glasses by sol–gel methods has proved to be difficult. This work reports a new sol–gel process for the production of Na2O-containing bioactive glass ceramics, potentially enabling their use as medical implantation materials. Fine powders of 45S5 (a Na2O-containing composition) glass ceramic have for the first time been successfully synthesized using the sol–gel technique in aqueous solution under ambient conditions, with the mean particle size being ∼5μm. A comparative study of sol–gel derived S70C30 (a Na2O-free composition) and 45S5 glass ceramic materials revealed that the latter possesses a number of features desirable in biomaterials used for bone tissue engineering, including (i) the crystalline phase Na2Ca2Si3O9 that couples good mechanical strength with satisfactory biodegradability, (ii) formation of hydroxyapatite, which may promote good bone bonding and (iii) cytocompatibility. In contrast, the sol–gel derived S70C30 glass ceramic consisted of a virtually inert crystalline phase CaSiO3. Moreover, amorphous S70C30 largely transited to CaCO3 with minor hydroxyapatite when immersed in simulated body fluid under standard tissue culture conditions. In conclusion, sol–gel derived Na2O-containing glass ceramics have significant advantages over related Na2O-free materials, having a greatly improved combination of mechanical capability and biological absorbability. [Copyright &y& Elsevier]

Abstract: Salvia miltiorrhiza is a medicinal herb commonly used in traditional Chinese medicine for the prevention and treatment of cardiovascular disease. This study investigated the effects of Cardiotonic Pill (CP), a pharmaceutical preparation of Salvia miltiorrhiza, on cardiac myocytes and fibroblasts with respect to the viability, proliferation, and collagen synthesis in these cells under various conditions. A cardiac myocyte line, H9c2, and primarily cultured fibroblasts from rat hearts were incubated with CP over a broad concentration range (50–800μg/ml) under normal cultures, conditions of ischemia (serum-free culture), and stimulation by angiotensin II (AII, 100nM), hydrogen peroxide (H2O2, 50–200μM), or tumor necrosis factor α (TNFα, 40ng/ml) for 24–48h. Cell growth, apoptosis, DNA and collagen synthesis, and expression of relevant genes were assessed via cell number study, morphological examination, Annexin-V staining, flow-cytometry, [3H]-thymidine or [3H]-proline incorporation assay, and Western blotting analysis. It was found that (1) at therapeutic (50μg/ml) and double therapeutic (100μg/ml) concentrations, CP did not significantly affect normal DNA synthesis and cell growth in these cardiac cells, while at higher (over 4-fold therapeutic) concentrations (200–800μg/ml), CP decreased DNA synthesis and cell growth and increased cell death; (2) CP treatment (50μg/ml) significantly inhibited TNFα-induced apoptosis in myocytes, with 12.3±1.46% cells being apoptosis in CP treatment group and 37.0±7.34% in the control (p<0.01), and simultaneously, expression of activated (phosphorylated) Akt protein was increased by about 2 folds in the CP-treated cells; and (3) in cultured fibroblasts, CP significantly reduced AII-induced collagen synthesis in a concentration-dependent manner (by ∼50% and ∼90% reduction of AII-induced collagen synthesis at 50 and 100μg/ml, respectively). Thus, Salvia miltiorrhiza preparation CP is physiologically active on cardiac cells. The actions by CP to reduce apoptotic damage in myocytes and collagen synthesis in fibroblasts may help to preserve the heart function and reduce heart failure risk. The actions by CP to inhibit DNA synthesis and cell growth, which occurred at over therapeutic doses, may weaken the ability of heart repair. Further studies are needed to identify the chemical compounds in this herbal product that are responsible for these observed physiological effects. [Copyright &y& Elsevier]

Aims Cellular and molecular mechanisms underlying the effects of androgenic hormone testosterone on the heart remain unclear. This study examined the impact of testosterone on viability of cardiac myocytes and the role of NF-κB signalling pathways. Materials and methods Rat H9c2 myocytes were cultured in steroid-free media and incubated with hydrogen peroxide (H 2 O 2 , 200 μM, 6 h). NF-κB expression was knocked down by RelA (p65) siRNA interference. Testosterone (5–100 nM, 24–48 h) was provided into the media and androgen receptor (AR) blocked by flutamide (100 nM). Cell apoptotic/necrotic death was determined by morphological examination and flow-cytometric analysis. Gene expression was examined by Western blotting analysis. Key findings Testosterone supplements reduced the superoxide-induced apoptotic/necrotic death, stimulated NF-κB (RelA) expression, activated Akt activity, and inhibited Caspase-3 expression in the cardiac myocytes. The hormonal effects were abolished by either AR blocker flutamide or NF-κB-knockdown. Testosterone also induced ERK1/2 activation, which was not affected by flutamide or NF-κB knockdown, and blocking the ERK activity did not affect the protective effect of the hormone on the cells. Significance This study demonstrates that exogenous testosterone supplementation protects cardiac myocytes from superoxide injury via AR mediation and dependent on normally functional canonical NF-κB (RelA/p50) signalling pathways. The NF-κB signalling may be an important key molecular basis for myocardial benefits of hormone (testosterone) therapy. [ABSTRACT FROM AUTHOR]

The media play a key role in promoting the thin ideal. A qualitative study, in which we used in depth interviews and thematic analysis, was undertaken to explore the attitudes of 142 obese individuals toward media portrayals of the thin ideal. Participants discussed the thin ideal as a social norm that is also supported through the exclusion of positive media portrayals of obese people. They perceived the thin ideal as an 'unhealthy' mode of social control, reflecting on their personal experiences and their concerns for others. Participants' perceptions highlighted the intersections between the thin ideal and gender, grooming and consumerism. Participants' personal responses to the thin ideal were nuanced e some were in support of the thin ideal and some were able to critically reflect and reject the thin ideal. We consider how the thin ideal may act as a form of synoptical social control, working in tandem with wider public health panoptical surveillance of body weight. [ABSTRACT FROM AUTHOR]

Abstract: Androgenic hormones are associated with atherosclerotic cardiovascular disease, although the underlying cellular and molecular mechanisms remain unclear. This study examines the impact of androgens on the physiology of human vascular endothelial cells (EC) and smooth muscle cells (SMC) in culture. Cells were incubated with testosterone, dihydrotestosterone (DHT) or dehydroepiandrosterone (DHEA) at various physiological concentrations (5–50nM) in the present or absence of an androgen receptor (AR) blocker flutamide (100nM). Cell growth and death, DNA and collagen synthesis, and gene protein expression were assessed. It was shown that: (1) DHEA protected EC from superoxide injury via AR-independent mechanisms; (2) testosterone induced DNA synthesis and growth in EC via an AR-independent manner with activation of ERK1/2 activity; (3) DHT inhibited DNA synthesis and growth in EC in an AR-dependent manner; (4) testosterone and DHT enhanced ERK1/2 activation and proliferation in SMC via AR-independent and -dependent pathways, respectively; and (5) these androgens did not significantly affect collagen synthesis in SMC. We conclude that androgens possess multiple effects on vascular cells via either AR-dependent or -independent mechanisms. Testosterone and DHEA may be “beneficial” in preventing atherosclerosis by improving EC growth and survival; in contrast, stimulation of VSMC proliferation by testosterone and DHT is potentially “harmful”. The relationship of these in vitro effects by androgens to in vivo vascular function and atherogenesis needs to be further clarified. [Copyright &y& Elsevier]

Abstract: Obesity stigma exists within many institutions and cultural settings. Most studies suggest that stigmatising experiences have a negative impact on individuals’ health and social behaviours and outcomes. However, some studies indicate that obesity stigma can motivate individuals to lose weight. Limited research has examined weight-based stigma from the perspective of obese individuals, including their perceptions of, and responses to, the different types of weight-based stigma they face in their daily lives. This study advances knowledge about weight-based stigma by documenting how obese adults (mostly female) described the different types of obesity stigma that they faced, how they responded to this stigma, and how different types of stigma impact on health and social wellbeing. Semi-structured, qualitative interviews were conducted between April 2008 and March 2009 with a diverse sample of 141 obese Australian adults. Guided by categorisation of different types of discrimination, participants’ experiences could be grouped into three distinct types of stigma: 1) Direct (e.g. being abused when using public transport); 2) Environmental (e.g. not being able to fit into seats on planes); and 3) Indirect (e.g. people staring at the contents of their supermarket trolley). Participants described that more subtle forms of stigma had the most impact on their health and social wellbeing. However, it was the interaction between direct, environmental and indirect stigma that created a barrier to participation in health-promoting activities. Participants rarely challenged stigma and often blamed themselves for stigmatising experiences. They also avoided situations where they perceived they would be stigmatised and constantly thought about how they could find a solution to their obesity. [Copyright &y& Elsevier]

Abstract: Background: Danshen (DS, Salvia miltiorrhiza), Shanchi (SQ, Panax notoginseng), Shanzai (SZ, Hawthorn) and Heshouwu (HSW, Polygonum multiflorum Thunb) are four medicinal herbs commonly used in traditional Chinese medicine and previously shown to have activity that may contribute to cardiovascular protection. This study aims to investigate effects of these herbs on vascular endothelial cells with respect to cell viability and expression of cellular adhesion molecules under inflammatory conditions. Methods: Herbal extracts were prepared by an established industrial manufacturing process. Human umbilical vein endothelial cells (HUVEC) were incubated with the herbal extract under normal or serum-free culture and tumor necrosis factor (TNF) α stimulation. Cell apoptosis, apoptosis-associated gene expression, expression of cellular adhesion molecules, DNA synthesis, and growth were assessed via morphological examination, Annexin-V staining, Western blotting analysis, Flow-Cytometry, [3H]-thymidine incorporation assay, and cell number study. Results: SZ and HSW significantly inhibited apoptosis in HUVEC undergoing serum deprivation and TNFα stimulation, accompanied by down-regulation of caspase-3 gene expression. DS and SQ significantly attenuated TNFα-induced expression of adhesion molecule VCAM-1 and also ICAM-1 by DS in the cells. All four herbs at therapeutic concentrations (100 μg/mL) inhibited DNA synthesis (10–42% decrease in [3H]-thymidine incorporation rates) and growth (5–10% decrease in cell numbers) in HUVEC under normal cultures. Conclusion: DS, SQ, SZ and HSW are physiologically active on human vascular endothelial cells. The actions by HSW and SZ to reduce apoptosis and DS and SQ to inhibit adhesion molecule expression may help protect endothelial function and inhibit atherogenesis, while their actions to inhibit DNA synthesis and cell growth may weaken the ability of endothelial repair. Further studies are needed to identify the chemical compounds responsible to these physiological effects by these herbs. [Copyright &y& Elsevier]

Abstract: Vascular endothelial cell (EC) integrity is key to arterial health; endothelial dysfunction is linked to atherogenesis. Atherosclerosis shows a male preponderance, possibly related to the protective effect of estrogens in women. This study examined the effect of estrogens on growth, apoptosis and adhesion molecule expression in cultured human EC. The effects of 17β-estradiol (E2) were studied in human umbilical vein endothelial cells (HUVEC) under normal culture conditions, and following exposure to cyclic mechanical strain or tumor necrosis factor α (TNFα). E2 enhanced HUVEC growth in serum-enriched media, in a concentration-dependent manner. This up-regulation of EC growth by E2 was associated with an increase in telomerase activity, assessed by PCR-based TRAP analysis. Cyclic strain enhanced [3H]-thymidine incorporation into DNA, and increased activation of mitogen-activated protein (MAP) kinase ERK1/2 and expression of early growth genes (Egr-1 and Sp-1); E2 attenuated the strain-induced ERK1/2 activation but not the early growth gene expression or DNA synthesis. TNFα (20ng/mL) induced apoptosis in HUVEC, causing a decrease in DNA synthesis, increase in floating and Annexin-V-stained cell numbers, and morphological changes. TNFα also upregulated ERK1/2 activity and expression of adhesion molecules (ICAM-1, VCAM-1 and E-selectin). E2 significantly attenuated the effects of TNFα on ERK1/2 activity, apoptosis, and E-selectin expression in the cells. Thus, estradiol enhances growth and reduces TNFα-induced apoptosis in EC; enhanced EC growth may be mediated via upregulation of telomerase activity. These effects are possible cellular mechanisms underlying female gender-associated cardiovascular protection. [Copyright &y& Elsevier]

Abstract: Stress is an important contributor to cardiovascular disease and to reduced immunity and fertility. As the role of androgens in stress is uncertain, we investigated the effects of testosterone (T) on hormonal responses to stress in conscious Romney Marsh wethers. Six T-treated sheep and six control sheep were stressed by exposure to a psychological and a metabolic stimulus. Baseline glucose levels were significantly lower in the treated animals compared with controls (p=0.002). T treatment significantly attenuated ACTH (p<0.01) and cortisol (p<0.05) responses to metabolic stress. Following psychological stress, ACTH responses were significantly lower in treated sheep compared with controls (p<0.05), but differences in mean cortisol responses did not reach significance. There were no significant differences in epinephrine or norepinephrine responses following either stressor. We conclude that T replacement in wethers lowers glucose and attenuates responses to metabolic and psychological stress. While the implications of these results for human physiology require further studies, they suggest that male hypogonadism may play a role in determining the risk of cardiovascular disease and diabetes. [Copyright &y& Elsevier]