Explore the vast range of titles available.

The mechanisms through which estrogen prevents bone loss are uncertain. Elsewhere, estrogen exerts beneficial actions by suppression of reactive oxygen species (ROS). ROS stimulate osteoclasts, the cells that resorb bone. Thus, estrogen might prevent bone loss by enhancing oxidant defenses in bone. We found that glutathione and thioredoxin, the major thiol antioxidants, and glutathione and thioredoxin reductases, the enzymes responsible for maintaining them in a reduced state, fell substantially in rodent bone marrow after ovariectomy and were rapidly normalized by exogenous 17-beta estradiol. Moreover, administration of N-acetyl cysteine (NAC) or ascorbate, antioxidants that increase tissue glutathione levels, abolished ovariectomy-induced bone loss, while l-buthionine-(S,R)-sulphoximine (BSO), a specific inhibitor of glutathione synthesis, caused substantial bone loss. The 17-beta estradiol increased glutathione and glutathione and thioredoxin reductases in osteoclast-like cells in vitro. Furthermore, in vitro NAC prevented osteoclast formation and NF-kappaB activation. BSO and hydrogen peroxide did the opposite. Expression of TNF-alpha, a target for NF-kappaB and a cytokine strongly implicated in estrogen-deficiency bone loss, was suppressed in osteoclasts by 17-beta estradiol and NAC. These observations strongly suggest that estrogen deficiency causes bone loss by lowering thiol antioxidants in osteoclasts. This directly sensitizes osteoclasts to osteoclastogenic signals and entrains ROS-enhanced expression of cytokines that promote osteoclastic bone resorption.

The mechanisms through which estrogen prevents bone loss are uncertain. Elsewhere, estrogen exerts beneficial actions by suppression of reactive oxygen species (ROS). ROS stimulate osteoclasts, the cells that resorb bone. Thus, estrogen might prevent bone loss by enhancing oxidant defenses in bone. We found that glutathione and thioredoxin, the major thiol antioxidants, and glutathione and thioredoxin reductases, the enzymes responsible for maintaining them in a reduced state, fell substantially in rodent bone marrow after ovariectomy and were rapidly normalized by exogenous 17-beta estradiol. Moreover, administration of N-acetyl cysteine (NAC) or ascorbate, antioxidants that increase tissue glutathione levels, abolished ovariectomy-induced bone loss, while l-buthionine-(S,R)-sulphoximine (BSO), a specific inhibitor of glutathione synthesis, caused substantial bone loss. The 17-beta estradiol increased glutathione and glutathione and thioredoxin reductases in osteoclast-like cells in vitro. Furthermore, in vitro NAC prevented osteoclast formation and NF-kappaB activation. BSO and hydrogen peroxide did the opposite. Expression of TNF-alpha, a target for NF-kappaB and a cytokine strongly implicated in estrogen-deficiency bone loss, was suppressed in osteoclasts by 17-beta estradiol and NAC. These observations strongly suggest that estrogen deficiency causes bone loss by lowering thiol antioxidants in osteoclasts. This directly sensitizes osteoclasts to osteoclastogenic signals and entrains ROS-enhanced expression of cytokines that promote osteoclastic bone resorption.The mechanisms through which estrogen prevents bone loss are uncertain. Elsewhere, estrogen exerts beneficial actions by suppression of reactive oxygen species (ROS). ROS stimulate osteoclasts, the cells that resorb bone. Thus, estrogen might prevent bone loss by enhancing oxidant defenses in bone. We found that glutathione and thioredoxin, the major thiol antioxidants, and glutathione and thioredoxin reductases, the enzymes responsible for maintaining them in a reduced state, fell substantially in rodent bone marrow after ovariectomy and were rapidly normalized by exogenous 17-beta estradiol. Moreover, administration of N-acetyl cysteine (NAC) or ascorbate, antioxidants that increase tissue glutathione levels, abolished ovariectomy-induced bone loss, while l-buthionine-(S,R)-sulphoximine (BSO), a specific inhibitor of glutathione synthesis, caused substantial bone loss. The 17-beta estradiol increased glutathione and glutathione and thioredoxin reductases in osteoclast-like cells in vitro. Furthermore, in vitro NAC prevented osteoclast formation and NF-kappaB activation. BSO and hydrogen peroxide did the opposite. Expression of TNF-alpha, a target for NF-kappaB and a cytokine strongly implicated in estrogen-deficiency bone loss, was suppressed in osteoclasts by 17-beta estradiol and NAC. These observations strongly suggest that estrogen deficiency causes bone loss by lowering thiol antioxidants in osteoclasts. This directly sensitizes osteoclasts to osteoclastogenic signals and entrains ROS-enhanced expression of cytokines that promote osteoclastic bone resorption.

Many Australians are deeply dissatisfied with the current situation in government schools. One possible solution is to try to create a uniform system markedly better than the present one by top-down legislation or regulations. This may not be impossible, and should be part of an overall policy, but it is very difficult to accomplish. The first reason is because diversities and incompatibilities of belief make moral vacuity an almost inevitable consequence of attempted uniformity. The second is that many government schoolteachers will sabotage attempted reforms with impunity. Just imagine the grimacing and adverse body language of many government schoolteachers as the flag of Australia is raised at school assembly. Curriculum committees will remain under the control of the very people whose influence has been so malignant in the past. Difficult as it would be, indeed an exploration of new ground, we should aim at bottom-up reform that makes possible a diverse school system that reflects the diversity of the Australian people. This would be a multiculturalism that liberals could take to their hearts.

ABSTRACT The paper considers the implications of the concept of the essential contestability of education for the professional independence of teachers. Its conclusion is that liberal educational ideas provide the strongest theoretical framework for such independence, with child-centred ideas a not very close second. Potential dangers to teachers' professional autonomy from transcendentalist, instrumentalist and reconstructionist theories of education are highlighted. The paper does not endorse unlimited contestability or unrestricted professional independence for teachers and outlines conditions, related to the Paradox of Freedom, in which restrictions are fully justifiable. However, it concludes that in contemporary liberal-democratic societies constraints on educational contestability should be as minimal as possible.

One of the many fascinating problems raised in recent issues of the Australian Journal of Indigenous Education (AJIE) is that of Indigenous autonomy in education. Although opinions differed about the extent to which Indigenous people currently exercise educational autonomy in various situations, there was wide agreement that there ought to be Indigenous control or ‘ownership’ of all knowledge relating to Indigenous life and culture, past and present. Sister Anne Gardner, then Principal of Murrupurtyanuwu Catholic School in NT, explained (1996: 20) how she decided to ‘let go, to move away from the dominant role as Principal’, in order that Indigenous persons could take control. She had been helped to this conclusion by reading Paulo Freire, Martin Buber and Hedley Beare, and, within the NT itself, ‘people of that educational calibre, such as Beth Graham, Sr Teresa Ward, Fran Murray, Stephen Harris, all pleading with us to allow education to be owned by Aboriginal people’. Sr Gardner held that ‘Aboriginal people never act as “leader”, a view shared by her designated Indigenous successor, Teresita Puruntayemeri, then Principal-in-Training of Murrupurtyanuwu Catholic School, who wrote (1996: 24-25) that ‘for a Tiwi peron it is too difficult to stand alone in leadership’. One way to share the burdens of leadership is, she suggests, to ‘perform different dances in the Milmaka ring, sometimes in pairs or in a group’.

Debate continues about how dividend imputation affects equity markets. Central issues are whether franking credits are 'priced' by the market, and how imputation influences the behaviours of market participants. We argue that the presence of imputation affects investor and corporate behaviour, and that it would be dangerous to assume imputation has no effect on prices because they are entirely determined in global markets. Focusing on the impact on corporate behaviour, especially with regard to dividend payout and capital structure policies, we conclude that imputation matters and it has probably been beneficial.

The author distinguishes between \"high-doctrine\" and \"low doctrine\" schools, noting that diverse populations have pushed the moral education in the public schools of many countries towards a \"low doctrine\" that avoids any activity or moral advocacy not shared by every social group. The author believes that public schools should restore the features of the former \"civil religion\" which reinforced the values of most parents (reform from above). However, given the difficulties the public schools are currently having in delivering a positive and cohesive set of basic values, he believes that parental choice in schools (reform from below) should be implemented. It should improve the quality of education and the achievement of students.