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Online learning has an important place in widening access and participation in higher education for diverse student cohorts. One cohort taking up online study in increasing numbers is that of mature- age, first-in-family students. First-in-family is defined as those who are the first in their immediate family, including parents, siblings, partners and children, to undertake university studies. This paper looks at the experience of 87 first-in-family students, for whom the opportunity to study open-entry, online undergraduate units through Open Universities Australia made it possible for them to embark on a university education. Using a qualitative methodology, in-depth interviews and surveys were conducted with these students as part of a wider study into first-in-family students. Findings include the important role that opportunity plays in providing the impetus for study, as well as the importance of support and encouragement from family, friends, colleagues and institutions in being able to continue the journey. [Author abstract, ed]

A review of the violent knife crime literature suggests that the experiential perspective is one which has not been addressed in academic study. The research presented hereafter aims to address this literary gap and generate transferable knowledge relevant to the lived experience of violent knife crime. The experiential study of the single case within psychological research involves detailed examination of a particular event. Participant ‘J’ is the survivor of an extremely violent attack, involving the use of a knife, in his own home. J’s experience was analysed using Interpretative Phenomenological Analysis with reference to elements of the lifeworld: temporality, spatiality, intersubjectivity, and embodiment. Three themes were identified: 1. switching from past to present tense when relaying traumatic experience; 2. The presence of redemption sequences; and 3. making sense as a temporal process, which included an additional two subthemes—‘The long journey’ and ‘Seeking belongingness’. This case emphasises that the traumatic event is conceptualised as one part of a longer journey towards recovery, and that recovery itself is central to the experience of violent knife crime. Finally, the need to understand recovery as temporal process highlights the need to provide victims with appropriate support in order to avoid negative outcomes.

Online learning has an important place in widening access and participation in higher education for diverse student cohorts. One cohort taking up online study in increasing numbers is that of mature-age, first-in-family students. First-in-family is defined as those who are the first in their immediate family, including parents, siblings, partners and children, to undertake university studies. This paper looks at the experience of 87 first-in-family students, for whom the opportunity to study open-entry, online undergraduate units through Open Universities Australia made it possible for them to embark on a university education. Using a qualitative methodology, in-depth interviews and surveys were conducted with these students as part of a wider study into first-in-family students (O'Shea, May & Stone, 2015). Findings include the important role that opportunity plays in providing the impetus for study, as well as the importance of support and encouragement from family, friends, colleagues and institutions in being able to continue the journey.

Online learning has an important place in widening access and participation in higher education for diverse student cohorts. One cohort taking up online study in increasing numbers is that of mature-age, first-in-family students. First-in-family is defined as those who are the first in their immediate family, including parents, siblings, partners and children, to undertake university studies. This paper looks at the experience of 87 first-in-family students, for whom the opportunity to study open-entry, online undergraduate units through Open Universities Australia made it possible for them to embark on a university education. Using a qualitative methodology, in-depth interviews and surveys were conducted with these students as part of a wider study into first-in-family students (O'Shea, May and Stone, 2015). Findings include the important role that opportunity plays in providing the impetus for study, as well as the importance of support and encouragement from family, friends, colleagues and institutions in being able to continue the journey.

Online learning has an important place in widening access and participation in higher education for diverse student cohorts. One cohort taking up online study in increasing numbers is that of mature-age, first-in-family students. First-in-family is defined as those who are the first in their immediate family, including parents, siblings, partners and children, to undertake university studies. This paper looks at the experience of 87 first-in-family students, for whom the opportunity to study open-entry, online undergraduate units through Open Universities Australia made it possible for them to embark on a university education. Using a qualitative methodology, in-depth interviews and surveys were conducted with these students as part of a wider study into first-in-family students (O'Shea, May and Stone, 2015). Findings include the important role that opportunity plays in providing the impetus for study, as well as the importance of support and encouragement from family, friends, colleagues and institutions in being able to continue the journey.

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.

Validated protocols for diagnostic testing and management of pregnant women with cardiovascular disease (CVD) do not exist. Our objective was to establish a prospective standardized protocol for the clinical evaluation of pregnant women with CVD. The Standardized Outcomes in Reproductive Cardiovascular Care (STORCC) initiative prospectively enrolled pregnant women with CVD into a standardized diagnostic testing and assessment protocol. Detailed cardiac and obstetric data were collected during the antepartum, intrapartum, and postpartum periods. Each woman was assigned a STORCC color code of perceived risk at a monthly multidisciplinary conference. In 250 pregnancies of 207 women with CVD, the standardized care protocol was followed in 136 and routine care in 114. The median age of the subjects was 32 years, and the most common form of heart disease was congenital heart disease (77%). Women enrolled in standardized care protocol had high compliance with second- and third-trimester visits (93%) and postpartum visits (76%). Maternal cardiac complications occurred in 10%. The STORCC cardiac and obstetric color codes predicted adverse outcomes within each respective category (P = .02, .01). The STORCC protocol for prospective diagnostic testing and follow-up of pregnant women with CVD was successfully established, and compliance was high. The strength of a standardized testing and care protocol as well as detailed classification of labor and delivery characteristics allows for robust analyses into specific questions regarding testing protocols, and mode and timing of delivery.

Electrocardiograms (EKGs) are routinely performed in pregnant patients with pre-existing cardiovascular disease. However, in pregnant patients with congenital heart disease (CHD), EKG changes during gestation have not been explored.BACKGROUNDElectrocardiograms (EKGs) are routinely performed in pregnant patients with pre-existing cardiovascular disease. However, in pregnant patients with congenital heart disease (CHD), EKG changes during gestation have not been explored.We performed a retrospective study of pregnant patients with CHD enrolled in the STORCC initiative. Patients were included if they had at least two EKGs across the perinatal period and were grouped by specific conditions: atrial septal defect (ASD), tetralogy of Fallot, congenital pulmonary stenosis, coarctation of the aorta (CoA), bicuspid aortic valve (BAV), systemic right ventricle (SRV), and Fontan circulation. EKG parameters were measured in all available EKGs by two investigators, blinded to diagnosis and time of gestation.METHODSWe performed a retrospective study of pregnant patients with CHD enrolled in the STORCC initiative. Patients were included if they had at least two EKGs across the perinatal period and were grouped by specific conditions: atrial septal defect (ASD), tetralogy of Fallot, congenital pulmonary stenosis, coarctation of the aorta (CoA), bicuspid aortic valve (BAV), systemic right ventricle (SRV), and Fontan circulation. EKG parameters were measured in all available EKGs by two investigators, blinded to diagnosis and time of gestation.One hundred and seventy pregnant patients were included. There was a statistically significant increase in HR from pre-pregnancy to third trimester in all groups except for those with Fontan and SRV. Patients with ASD and BAV had a statistically significant increase in their QTc (ASD:13 ms, p = 0.017; BAV:7 ms, p = 0.018) during pregnancy. QRS duration was shorter (4 ms) in the third trimester for patients with ASD (p = 0.033) and CoA (p = 0.014). Despite these individual findings, EKG parameters remained within normal limits and regressed to baseline in the postpartum period.RESULTSOne hundred and seventy pregnant patients were included. There was a statistically significant increase in HR from pre-pregnancy to third trimester in all groups except for those with Fontan and SRV. Patients with ASD and BAV had a statistically significant increase in their QTc (ASD:13 ms, p = 0.017; BAV:7 ms, p = 0.018) during pregnancy. QRS duration was shorter (4 ms) in the third trimester for patients with ASD (p = 0.033) and CoA (p = 0.014). Despite these individual findings, EKG parameters remained within normal limits and regressed to baseline in the postpartum period.Patients with CHD have statistically significant EKG changes throughout pregnancy, but the values remain within normal limits. Like patients without heart disease, those with CHD increase their HR during pregnancy, except individuals with SRV and Fontan, who appear to lack capacity for physiologic HR augmentation.CONCLUSIONSPatients with CHD have statistically significant EKG changes throughout pregnancy, but the values remain within normal limits. Like patients without heart disease, those with CHD increase their HR during pregnancy, except individuals with SRV and Fontan, who appear to lack capacity for physiologic HR augmentation.

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.