28 research outputs found
Chinese Economic Development
No full textThis book outlines and analyzes the economic development of China between 1949 and 2007. Rather than being narrowly economic, the book addresses many of the broader aspects of development, including literacy, morality, demographics and the environment. The distinctive features of this book are its sweep and that it does not shy away from controversial issues. For example, there is no question that aspects of Maoism were disastrous but Bramall argues that there was another side to the whole programme. More recently, the current system of government has presided over three decades of very rapid economic growth. However, the author shows that this growth has come at a price. Bramall makes it clear that unless radical change takes place, Chinese growth will not be sustainable. This large, comprehensive text is relevant to all those studying the economic history of China as well as its contemporary economy. It is also useful more generally for students and researchers in the fields of international and development economics
Ankrd11 is a chromatin regulator involved in autism that is essential for neural development
No full textAbstract not availableDenis Gallagher, Anastassia Voronova, Mark A. Zander, Gonzalo I. Cancino, Alexa Bramall, Matthew P. Krause, Clemer Abad, Mustafa Tekin, Paul M. Neilsen, David F. Callen, Stephen W. Scherer, Gordon M. Keller, David R. Kaplan, Katherina Walz, and Freda D. Mille
This Conjuncture: Patriarchy in the digital conjuncture
No full textNew Formations This Conjuncture seminar series.
The fifth of a series of online seminars hosted by the journal New Formations in Autumn 2021, organised by Rebecca Bramall and Jeremy Gilbert. The series marks the publication of the journal’s series of issues published under the title This Conjuncture and dedicated to the memory of Stuart Hall.
Patriarchy in the digital conjuncture
Digital platforms create new opportunities to express misogyny in increasingly extreme ways, intersect with the structures of patriarchy sustained in everyday life. In the form of misogynistic ‘rationalism’, these ideas also permeate the culture of Silicon Valley. Join Sarah Banet-Weiser, Ben Little and Alison Winch to discuss networked misogyny and male victimhood in the context of the growing power and influence of digital platforms.
Speakers:
Sarah Banet-Weiser is Distinguished Professor of Communication and Director of the Annenberg Centre for Collaborative Communication. Her books include Authentic™: The Politics of Ambivalence in a Brand Culture (2012), and Empowered: Popular Feminism and Popular Misogyny (2018).
Ben Little is Lecturer in Media and Cultural Politics at the University of East Anglia. He is the co-author of The New Patriarchs of Digital Capitalism (2021) and Russell Brand: Comedy, Celebrity and Politics (2016, with Jane Arthurs).
Alison Winch is Lecturer in Media Studies at the University of East Anglia. Her books include The New Patriarchs of Digital Capitalism (2021) and Girlfriends and Postfeminist Sisterhood (2013). Alison and Ben are the authors of ‘Patriarchy in the digital conjuncture – an analysis of Google’s James Damore’, which was published as part of This Conjuncture
Elucidating the Role of Endothelin-2 (ET-2) in Inherited Photoreceptor Degenerations and the Indirect Effects of Systemic ET-2 Loss
No full textInherited photoreceptor degenerations (IPDs) are the most common monogenic cause of blindness in humans. To discover genes that may influence the risk of death in IPDs, microarray studies were used, and ET-2 was identified as the most differentially expressed transcript. ET-2 mRNA was 32-fold (p0.05), suggesting that the rescue observed in vivo might be due to extraocular mechanisms. Additionally, the expression of ET-2 mRNA from an rAAV5-CBA-ET-2 vector in ET-2-/-; Rd1-/- retinas did not restore PR degeneration (n=6;p>0.05). A survey of the extraocular phenotypes of ET-2 null mice showed them to be hypoxic owing to aberrant lung development, with a loss of normal alveolarization of the lung. Erythropoietin (EPO) levels were 11-fold elevated in the serum of ET-2 null mice (n=7;p<0.05) and retinal vascular endothelial growth factor (VEGF) was increased 4-fold (n=4;p<0.05). To examine the role of hypoxia in PR degeneration and to exclude increased EPO levels as the sole factor accounting for the rescue of mutant PRs in ET-2-/-; Tg(RHO P347S) and ET-2-/-;Rd1-/- mice in vivo, the effect of hypoxia on PR death in Rd1-/- retinal explants was examined. Rd1-/- explants cultured in 6% O2 from PN10 to PN17 showed a 32% rescue of PR death (n=5;p<0.05). Although ET-2 may mediate PR death through a direct role in mutant PRs, the PR rescue observed in ET-2-/-; Tg(RHO P347S) and ET-2-/-;Rd1-/-retinas may also result from systemic hypoxia due to poor lung function in ET-2-/- animals.Ph
Elucidating the Role of Endothelin-2 (ET-2) in Inherited Photoreceptor Degenerations and the Indirect Effects of Systemic ET-2 Loss
No full textInherited photoreceptor degenerations (IPDs) are the most common monogenic cause of blindness in humans. To discover genes that may influence the risk of death in IPDs, microarray studies were used, and ET-2 was identified as the most differentially expressed transcript. ET-2 mRNA was 32-fold (p0.05), suggesting that the rescue observed in vivo might be due to extraocular mechanisms. Additionally, the expression of ET-2 mRNA from an rAAV5-CBA-ET-2 vector in ET-2-/-; Rd1-/- retinas did not restore PR degeneration (n=6;p>0.05). A survey of the extraocular phenotypes of ET-2 null mice showed them to be hypoxic owing to aberrant lung development, with a loss of normal alveolarization of the lung. Erythropoietin (EPO) levels were 11-fold elevated in the serum of ET-2 null mice (n=7;p<0.05) and retinal vascular endothelial growth factor (VEGF) was increased 4-fold (n=4;p<0.05). To examine the role of hypoxia in PR degeneration and to exclude increased EPO levels as the sole factor accounting for the rescue of mutant PRs in ET-2-/-; Tg(RHO P347S) and ET-2-/-;Rd1-/- mice in vivo, the effect of hypoxia on PR death in Rd1-/- retinal explants was examined. Rd1-/- explants cultured in 6% O2 from PN10 to PN17 showed a 32% rescue of PR death (n=5;p<0.05). Although ET-2 may mediate PR death through a direct role in mutant PRs, the PR rescue observed in ET-2-/-; Tg(RHO P347S) and ET-2-/-;Rd1-/-retinas may also result from systemic hypoxia due to poor lung function in ET-2-/- animals.Ph
The genomic, biochemical, and cellular responses of the retina in inherited photoreceptor degenerations and prospects for the treatment of these disorders
No full textThe association of more than 140 genes with human photoreceptor degenerations, together with studies of animal models of these monogenic diseases, has provided great insight into their pathogenesis. Here we review the responses of the retina to photoreceptor mutations, including mechanisms of photoreceptor death. We discuss the roles of oxidative metabolism, mitochondrial reactive oxygen species, metabolic stress, protein misfolding, and defects in ciliary proteins, as well as the responses of Muller glia, microglia, and the retinal vasculature. Finally, we report on potential pharmacologic and biologic therapies, the critical role of histopathology as a prerequisite to treatment, and the exciting promise of gene therapy in animal models and in phase 1 trials in humans. © 2010 by Annual Reviews. All rights reserved
Endothelin-2 deficiency causes growth retardation, hypothermia, and emphysema in mice
No full textTo explore the physiological functions of endothelin-2 (ET-2), we generated gene-targeted mouse models. Global Et2 knockout mice exhibited severe growth retardation and juvenile lethality. Despite normal milk intake, they suffered from internal starvation characterized by hypoglycemia, ketonemia, and increased levels of starvation-induced genes. Although ET-2 is abundantly expressed in the gastrointestinal tract, the intestine was morphologically and functionally normal. Moreover, intestinal epithelium-specific Et2 knockout mice showed no abnormalities in growth and survival. Global Et2 knockout mice were also profoundly hypothermic. Housing Et2 knockout mice in a warm environment significantly extended their median lifespan. However, neuron-specific Et2 knockout mice displayed a normal core body temperature. Low levels of Et2 mRNA were also detected in the lung, with transient increases soon after birth. The lungs of Et2 knockout mice showed emphysematous structural changes with an increase in total lung capacity, resulting in chronic hypoxemia, hypercapnia, and increased erythropoietin synthesis. Finally, systemically inducible ET-2 deficiency in neonatal and adult mice fully reproduced the phenotype previously observed in global Et2 knockout mice. Together, these findings reveal that ET-2 is critical for the growth and survival of postnatal mice and plays important roles in energy homeostasis, thermoregulation, and the maintenance of lung morphology and function.ope
Refining the diagnostic evaluation of idiopathic normal pressure hydrocephalus with Alzheimer's and α-synuclein biomarkers
No full textIdiopathic normal pressure hydrocephalus (iNPH), characterized by ventriculomegaly and Hakim's triad of gait disturbance, cognitive impairment, and urinary dysfunction, is common in older adults. iNPH also remains one of the few potentially reversible neurological conditions, typically treated with cerebrospinal fluid (CSF) shunting. Although many patients improve, shunt responsiveness varies widely (≈60%−90%), and a subset of patients show only transient benefit. A major contributor to this variability is the high prevalence of comorbid neurodegenerative disease with symptom overlap, particularly Alzheimer's disease (AD) and α-synucleinopathies such as Parkinson's disease (PD) and dementia with Lewy bodies (DLB). The impact of these concomitant conditions on shunt outcomes, however, remains uncertain. We describe the incorporation of AD CSF biomarkers and α-synuclein skin biopsy into the iNPH evaluation to identify coexisting pathology. When integrated into routine workflow, approximately 32% of patients demonstrated AD-consistent CSF profiles and 31% had biopsy-confirmed α-synuclein pathology. We propose adopting concomitant neurological testing, especially in patients with atypical features to help inform patient selection and guide expectations. As the awareness and potential prevalence of iNPH rises and shunt procedures carry meaningful complication risks, delineating how comorbid disease modifies outcomes will be essential to improving the long-term success of shunting in iNPH
