Private Health Insurance Provisions of H.R. 3962

[Excerpt] This report summarizes key provisions affecting private health insurance, including provisions to raise revenues, in Division A of H.R. 3962, the Affordable Health Care for America Act, as introduced in the House of Representatives on October 29, 2009. H.R. 3962 is based on H.R. 3200, America’s Affordable Health Choices Act of 2009, which was originally introduced on July 14, 2009, and was reported separately on October 14, 2009, by three House Committees— Education and Labor, Energy and Commerce, and Ways and Means. Division A of H.R. 3962 focuses on reducing the number of uninsured, restructuring the private health insurance market, setting minimum standards for health benefits, and providing financial assistance to certain individuals and, in some cases, small employers. In general, H.R. 3962 would require individuals to maintain health insurance and employers to either provide insurance or pay a payroll assessment, with some exceptions. Several insurance market reforms would be made, such as modified community rating and guaranteed issue and renewal. Both the individual and employer mandates would be linked to acceptable health insurance coverage, which would meet required minimum standards and incorporate the market reforms included in the bill. Acceptable coverage would include (1) coverage under a qualified health benefits plan (QHBP), which could be offered either through the newly created Health Insurance Exchange (the Exchange) or outside the Exchange through new employer plans; (2) grandfathered employment based plans; (3) grandfathered nongroup plans; and (4) other coverage, such as Medicare and Medicaid. The Exchange would offer private plans alongside a public option. Based on income, certain individuals could qualify for subsidies toward their premium costs and cost-sharing (deductibles and copayments); these subsidies would be available only through the Exchange. In the individual market (the nongroup market), a plan could be grandfathered indefinitely, but only if no changes were made to the terms and conditions of that plan, including benefits and cost-sharing, and premiums were only increased as allowed by statute. Most of these provisions would be effective beginning in 2013. The Exchange would not be an insurer; it would provide eligible individuals and small businesses with access to insurers’ plans in a comparable way. The Exchange would consist of a selection of private plans as well as a public option. Individuals wanting to purchase the public option or a private health insurance not through an employer or a grandfathered nongroup plan could only obtain such coverage through the Exchange. They would only be eligible to enroll in an Exchange plan if they were not enrolled in Medicare, Medicaid, and acceptable employer coverage as a full-time employee. The public option would be established by the Secretary of Health and Human Services (HHS), would offer three different cost-sharing options, and would vary premiums geographically. The Secretary would negotiate payment rates for medical providers, and items and services. The bill would also require that the Health Choices Commissioner to establish a Consumer Operated and Oriented Plan (CO-OP) program under which the Commissioner would make grants and loans for the establishment of not-for-profit, member-run health insurance cooperatives. These co-operatives would provide insurance through the Exchange. Only within the Exchange, credits would be available to limit the amount of money certain individuals would pay for premiums and for cost-sharing (deductibles and copayments). (Although Medicaid is beyond the scope of this report, H.R. 3962 would extend Medicaid coverage for most individuals under 150% of poverty; individuals would be ineligible for Exchange coverage if they were eligible for Medicaid.

Simon Terrill: Crowd Theory 2004-18, Perspectives, Notes and Comments

A catalogue publication for a major survey of the monumental Crowd Theory photographs by Melbourne-born, London-based artist Simon Terrill. The publication coincides with an exhibition bringing together all ten Crowd Theory images for the first time, at the Centre for Contemporary Photography, Melbourne. Inside are a range of responses and documents, including images and texts from the time of each event, as well as three newly commissioned essays reflecting on the project

Quantitative Proteomics Reveals a "Poised Quiescence" Cellular State after Triggering the DNA Replication Origin Activation Checkpoint

An origin activation checkpoint has recently been discovered in the G1 phase of the mitotic cell cycle, which can be triggered by loss of DNA replication initiation factors such as the Cdc7 kinase. Insufficient levels of Cdc7 activate cell cycle arrest in normal cells, whereas cancer cells appear to lack this checkpoint response, do not arrest, and proceed with an abortive S phase, leading to cell death. The differential response between normal and tumor cells at this checkpoint has led to widespread interest in the development of pharmacological Cdc7 inhibitors as novel anticancer agents. We have used RNAi against Cdc7 in combination with SILAC-based high resolution MS proteomics to investigate the cellular mechanisms underlying the maintenance of the origin activation checkpoint in normal human diploid fibroblasts. Bioinformatics analysis identified clear changes in wide-ranging biological processes including altered cellular energetic flux, moderate stress response, reduced proliferative capacity, and a spatially distributed response across the mitochondria, lysosomes, and the cell surface. These results provide a quantitative overview of the processes involved in maintenance of the arrested state, show that this phenotype involves active rather than passive cellular adaptation, and highlight a diverse set of proteins responsible for cell cycle arrest and ultimately for promotion of cellular survival. We propose that the Cdc7-depleted proteome maintains cellular arrest by initiating a dynamic quiescence-like response and that the complexities of this phenotype will have important implications for the continued development of promising Cdc7-targeted cancer therapies

Dietary restriction in ILSXISS mice is associated with widespread changes in splicing regulatory factor expression levels.

This is the author accepted manuscript. The final version is available from Elsevier via the DOI in this record Dietary restriction (DR) represents one of the most reproducible interventions to extend lifespan and improve health outcomes in a wide range of species, but substantial variability in DR response has been observed, both between and within species. The mechanisms underlying this variation in effect are still not well characterised. Splicing regulatory factors have been implicated in the pathways linked with DR-induced longevity in C. elegans and are associated with lifespan itself in mice and humans. We used qRT-PCR to measure the expression levels of a panel of 20 age- and lifespan-associated splicing regulatory factors in brain, heart and kidney derived from three recombinant inbred strains of mice with variable lifespan responses to short-term (2 months) or long-term (10 months) 40% DR to determine their relationship to DR-induced longevity. We identified 3 patterns of association; i) splicing factors associated with DR alone, ii) splicing factors associated with strain alone or iii) splicing factors associated with both DR and strain. Tissue specific variation was noted in response to short term or long-term DR, with the majority of effects noted in brain following long term DR in the positive responder strain TejJ89. Association in heart and kidney were less evident, and occurred following short term DR. Splicing factors associated with both DR and strain may be mechanistically involved in strain-specific differences in response to DR. We provide here evidence concordant with a role for some splicing factors in the lifespan modulatory effects of DR across different mouse strains and in different tissues

Algebraic description of spacetime foam

A mathematical formalism for treating spacetime topology as a quantum observable is provided. We describe spacetime foam entirely in algebraic terms. To implement the correspondence principle we express the classical spacetime manifold of general relativity and the commutative coordinates of its events by means of appropriate limit constructions.Comment: 34 pages, LaTeX2e, the section concerning classical spacetimes in the limit essentially correcte

Integrable Generalisations of the 2-dimensional Born Infeld Equation

The Born-Infeld equation in two dimensions is generalised to higher dimensions whilst retaining Lorentz Invariance and complete integrability. This generalisation retains homogeneity in second derivatives of the field.Comment: 11 pages, Latex, DTP/93/3

HMM based scenario generation for an investment optimisation problem

This is the post-print version of the article. The official published version can be accessed from the link below - Copyright @ 2012 Springer-Verlag.The Geometric Brownian motion (GBM) is a standard method for modelling financial time series. An important criticism of this method is that the parameters of the GBM are assumed to be constants; due to this fact, important features of the time series, like extreme behaviour or volatility clustering cannot be captured. We propose an approach by which the parameters of the GBM are able to switch between regimes, more precisely they are governed by a hidden Markov chain. Thus, we model the financial time series via a hidden Markov model (HMM) with a GBM in each state. Using this approach, we generate scenarios for a financial portfolio optimisation problem in which the portfolio CVaR is minimised. Numerical results are presented.This study was funded by NET ACE at OptiRisk Systems

Cnih3 deletion dysregulates dorsal hippocampal transcription across the estrous cycle

In females, the hippocampus, a critical brain region for coordination of learning, memory, and behavior, displays altered physiology and behavioral output across the estrous or menstrual cycle. However, the molecular effectors and cell types underlying these observed cyclic changes have only been partially characterized to date. Recently, profiling of mice null for the AMPA receptor trafficking gen