Bankruptcy and the Future of Aggregate Litigation: The Past as Prologue?

Part I of this Article recounts the development of the law of business reorganizations and the sustained attack on bankruptcy practice that culminated in the hobbling of the reorganization bar during the New Deal. I provide a good deal of detail about these historical developments, because they are largely unknown to those in the complex litigation field. Understanding the path of business reorganization law helps to situate the later lessons I draw from the parallels between bankruptcy and the class action. Part II recounts the movement to reform and revive bankruptcy practice, a movement that helped produce a new Bankruptcy Code in 1978. The Code reversed key policy decisions made in the New Deal era and, as a consequence, spurred a revival of corporate reorganizations in the late twentieth century. Part III draws from that background and attempts to sketch out briefly—more in the form of questions than definitive answers—possible routes for the future development of aggregate litigation

Master planned estates : parish or panacea?

Master planned estates in Australia emerge from two major directions: one aims to address the inadequacies of 1970s suburbanisation and the other comes from governments and developers seeking to realise alternatives. The very idea of master planning has a longer history, one that arguably dates back to 19th-century Utopian Socialism and Baron Haussmann\u27s redesign of Paris, which involved a large-scale, comprehensive alternative vision realised by a sanctioned authority. Master planning thereby partakes of both utopianism and authoritarianism. These associations have infused the discussion and construction of Australian master planned estates rendering them both pariah and panacea. But research and my own experience suggests that they are far more panaceas than pariahs

Software for the frontiers of quantum chemistry:An overview of developments in the Q-Chem 5 package

This article summarizes technical advances contained in the fifth major release of the Q-Chem quantum chemistry program package, covering developments since 2015. A comprehensive library of exchange–correlation functionals, along with a suite of correlated many-body methods, continues to be a hallmark of the Q-Chem software. The many-body methods include novel variants of both coupled-cluster and configuration-interaction approaches along with methods based on the algebraic diagrammatic construction and variational reduced density-matrix methods. Methods highlighted in Q-Chem 5 include a suite of tools for modeling core-level spectroscopy, methods for describing metastable resonances, methods for computing vibronic spectra, the nuclear–electronic orbital method, and several different energy decomposition analysis techniques. High-performance capabilities including multithreaded parallelism and support for calculations on graphics processing units are described. Q-Chem boasts a community of well over 100 active academic developers, and the continuing evolution of the software is supported by an “open teamware” model and an increasingly modular design

Cartilage-specific overexpression of ERRγ results in Chondrodysplasia and reduced chondrocyte proliferation.

While the role of estrogen receptor-related receptor alpha (ERRα) in chondrogenesis has been investigated, the involvement of ERR gamma (ERRγ) has not been determined. To assess the effect of increased ERRγ activity on cartilage development in vivo, we generated two transgenic (Tg) lines overexpressing ERRγ2 via a chondrocyte-specific promoter; the two lines exhibited ∼3 and ∼5 fold increased ERRγ2 protein expression respectively in E14.5 Tg versus wild type (WT) limbs. On postnatal day seven (P7), we observed a 4-10% reduction in the size of the craniofacial, axial and appendicular skeletons in Tg versus WT mice. The reduction in bone length was already present at birth and did not appear to involve bones that are derived via intramembranous bone formation as the bones of the calvaria, clavicle, and the mandible developed normally. Histological analysis of P7 growth plates revealed a reduction in the length of the Tg versus WT growth plate, the majority of which was attributable to a reduced proliferative zone. The reduced proliferative zone paralleled a decrease in the number of Ki67-positive proliferating cells, with no significant change in apoptosis, and was accompanied by large cell-free swaths of cartilage matrix, which extended through multiple zones of the growth plate. Using a bioinformatics approach, we identified known chondrogenesis-associated genes with at least one predicted ERR binding site in their proximal promoters, as well as cell cycle regulators known to be regulated by ERRγ. Of the genes identified, Col2al, Agg, Pth1r, and Cdkn1b (p27) were significantly upregulated, suggesting that ERRγ2 negatively regulates chondrocyte proliferation and positively regulates matrix synthesis to coordinate growth plate height and organization

Col2::ERRγ2 transgenic mouse generation and protein expression analysis.

<p>(A) ERR and ER gene expression (relative to L32) in adult mouse cartilage. Graphs represent mean ± SD from a minimum of 3 independent samples. (B) Schematic of the transgene used to express the long protein isoform, ERRγ2, in cartilage. Whole mount lacZ staining of a WT and transgenic 14.5 dpc embryo with a close-up of the forelimbs showing robust staining in the developing cartilage. Some nonspecific staining along the neural tube is evident. (C) Western blots and resulting quantification showing the levels of ERRγ and β-ACTIN proteins in 14.5 dpc limbs of the two transgenic lines compared to WT. Graphs represent the mean ± SD from at least three independent Western blots. **p≤0.01.</p

Decreased proliferation, but not apoptosis, is responsible for reduction of growth plate height.

<p>(A) Hoechst labeling and immunofluorescence of proximal humerus growth plate from WT and Line 2 samples, showing Ki67 positive cells in the proliferating zone (PZ) (red boxes), and resting zone (RZ) (white box). 2° Ab is a section stained with secondary antibody only and Hoechst. Lower panel shows the proliferative zone (red box) and part of the resting zone (blue box) under higher magnification, highlighting the difference in Ki67 positive cells within the proliferative zone of WT and Tg mice (B) Quantification of Ki67 positive cells from Line 2 proximal humerus growth plates demonstrated a clear reduction in the number of proliferating cells in the proliferating zone compared to the resting zone. WT (n = 6), Line 2 (n = 6); ***p≤0.001 (C) Quantification of TUNEL positive cells shows no difference in apoptotic cells in either the proliferating or hypertrophic zones. (D) Gene expression for apoptotic markers, <i>Bax</i> and <i>Bcl2,</i> from 14.5 dpc limbs confirms lack of increased apoptosis.</p