Submission to the Productivity Commission on Disability Care and Support

The authors of this submission welcome: • the proposal for a scheme to provide long term care and support on an entitlement basis, • many of the accompanying features of the approach outlined, including the no fault basis of provision, the inclusion of aids and equipment, and the recognition of the need to include the full range of support services, • the acknowledgment of unmet demand and the need for significant new funding.Centre for Disability Research and Polic

Submission to the Productivity Commission on Disability Care and Support 11 May 2011

The authors of this submission welcome the Productivity Commission (PC) Draft Report and many of the key features of the proposed NDIS including: • the proposal for a scheme to provide long term care and support on an entitlement basis, • many of the accompanying features of the approach outlined, including the no fault basis of provision, the inclusion of aids and equipment, and the recognition of the need to include the full range of support services, • the acknowledgment of unmet demand and the need for significant new funding. Our comments on the draft report are made in the spirit that we endorse the main directions of the proposed scheme, which would be of great benefit to the Australian people, most especially people with disabilities and their families. We sincerely hope that governments will respond positively and promptly to the vision laid out in the Draft Report. We offer constructive criticism to maximise the chances of the scheme’s success, in terms of enabling people to access the supports they need, on an equitable basis. In this submission we focus on 5 areas: 1. Eligibility and assessment 2. Assessment Tools 3. Overcoming access and equity barriers for Aboriginal communities 4. Research and Data 5. GovernanceCentre for Disability Research and Polic

A New Way to Measure the World's Protected Area Coverage

Protected areas are effective at stopping biodiversity loss, but their placement is constrained by the needs of people. Consequently protected areas are often biased toward areas that are unattractive for other human uses. Current reporting metrics that emphasise the total area protected do not account for this bias. To address this problem we propose that the distribution of protected areas be evaluated with an economic metric used to quantify inequality in income— the Gini coefficient. Using a modified version of this measure we discover that 73% of countries have inequitably protected their biodiversity and that common measures of protected area coverage do not adequately reveal this bias. Used in combination with total percentage protection, the Gini coefficient will improve the effectiveness of reporting on the growth of protected area coverage, paving the way for better representation of the world's biodiversity

Small-Group, Computer-Assisted Tutoring to Improve Reading Outcomes for Struggling First and Second Graders

This study evaluated the relative effects of Tier II computer-assisted tutoring in small groups (Team Alphie) and one-to-one tutoring provided to struggling readers in 33 high-poverty Success for All (SFA) schools. In this year-long study, struggling readers in the Team Alphie schools were tutored in groups of 6. In the control schools, students were tutored using the standard one-to-one tutoring process used in SFA. Analyses of covariance of students' standardized reading scores indicated that the first-grade treatment group significantly outperformed the control group on all 3 reading measures, with no significant differences for second graders. Schools using Team Alphie were able to tutor many more students than the control schools. This study shows that a computer-assisted, small-group tutoring program may be at least as effective as one-to-one tutoring and serve more struggling readers. It may serve as a good example of Tier II instruction in a response to intervention (RTI) model

ToTem: A phase Ib trial of temisirolimus with gemcitabine and cisplatin.

Background: gemcitabine (G) and cisplatin (C) is a standard-of-care, combination chemotherapy regimen for neoadjuvant treatment of muscle-invasive and palliative treatment of advanced bladder cancer (BC). More effective regimens are urgently needed, with no significant improvements on GC in more than a decade. Mammalian target of rapamycin (mTOR) is a rational target for BC therapy, as abnormalities are commonly seen in mTOR’s upstream activators/downstream effectors in the PI3K/AKT/mTOR signaling pathway. We therefore performed a Phase Ib trial, combining escalating doses of the mTOR inhibitor, temsirolimus (T) with GC. Methods: following regulatory and ethical approvals, eligible patients with advanced malignancy were treated with one or more doses of intravenous (IV) T plus fixed doses of IV GC in a 21-day (d) cycle. Previous unpublished data suggest a possible interaction between G and T. We therefore pursued a cautious escalation strategy (see table), as a precaution against excessive toxicity. Results: 14 patients (3 BC, 2 lung, 2 ovarian, 7 other cancers; 7 previous platinum exposure) were treated, at 4 dose schedules in 2 UK centers. There were no treatment-related deaths or SUSARs. Of 14 SAEs, 4 were SARs, in 10 individuals, 7 of whom had received IMP. Addition of 10mg T on d15, then d8&15 was tolerated, but DLTs were encountered when administering three 10mg doses of T, both on d1,8&15 (neutropenia; hypokalaemia) and d2,9&15 (febrile neutropenia; rash). T was omitted because of myelosuppression on d15, cycle 1 in 6/8 patients scheduled to receive 3 doses of T. Conclusions: it has not been feasible to add three, weekly doses of T to GC, even at low T doses, in the patient group tested, because of predominantly hematological toxicity. We plan to amend the schedule to include two doses of T, on d2&9, informed by data from pre-planned PK analyses of patients already treated. ToTem was developed by the UK NCRI Bladder Cancer Clinical Studies Group, sponsored by Cardiff University, funded by Cancer Research UK, and supported by supply of free drug and distribution costs from Pfizer. Clinical trial information: 31546330

Further Development of Verification Check-Cases for Six- Degree-of-Freedom Flight Vehicle Simulations

This follow-on paper describes the principal methods of implementing, and documents the results of exercising, a set of six-degree-of-freedom rigid-body equations of motion and planetary geodetic, gravitation and atmospheric models for simple vehicles in a variety of endo- and exo-atmospheric conditions with various NASA, and one popular open-source, engineering simulation tools. This effort is intended to provide an additional means of verification of flight simulations. The models used in this comparison, as well as the resulting time-history trajectory data, are available electronically for persons and organizations wishing to compare their flight simulation implementations of the same models

Conservation tillage systems for cotton advance in the San Joaquin Valley

Cotton production in the San Joaquin Valley has traditionally relied heavily on tillage for its presumed benefits to plant establishment, yields and insect management. Research in the 1960s and 1970s demonstrated the potential of precision or zone tillage, which foreshadowed the introduction of a variety of minimum tillage implements in the early 1990s. During a 3-year comparison study from 2001 to 2003, cotton yields in strip tillage plots matched or exceeded yields of standard tillage plots in all 3 years. In a 12-year study from 1999 to 2011, tillage costs were lowered an average of $70 per acre in 2011 dollars using no-tillage compared to standard tillage while achieving statistically comparable yields, provided that adequate crop stands were achieved. If bottom-line profitability can be maintained, conservation tillage may become increasingly attractive to cotton producers in the San Joaquin Valley

Australia\u27s health 2000 : the seventh biennial report of the Australian Institute of Health and Welfare

Australia\u27s Health 2000 is the seventh biennial health report of the Australian Institute of Health and Welfare. It is the nation\u27s authoritative source of information on patterns of health and illness, determinants of health, the supply and use of health services, and health services costs and performance.This 2000 edition serves as a summary of Australia\u27s health record at the end of the twentieth century. In addition, a special chapter is presented on changes in Australia\u27s disease profile over the last 100 years.Australia\u27s Health 2000 is an essential reference and information source for all Australians with an interest in health

Multiple Independent Loci at Chromosome 15q25.1 Affect Smoking Quantity: a Meta-Analysis and Comparison with Lung Cancer and COPD

Recently, genetic association findings for nicotine dependence, smoking behavior, and smoking-related diseases converged to implicate the chromosome 15q25.1 region, which includes the CHRNA5-CHRNA3-CHRNB4 cholinergic nicotinic receptor subunit genes. In particular, association with the nonsynonymous CHRNA5 SNP rs16969968 and correlates has been replicated in several independent studies. Extensive genotyping of this region has suggested additional statistically distinct signals for nicotine dependence, tagged by rs578776 and rs588765. One goal of the Consortium for the Genetic Analysis of Smoking Phenotypes (CGASP) is to elucidate the associations among these markers and dichotomous smoking quantity (heavy versus light smoking), lung cancer, and chronic obstructive pulmonary disease (COPD). We performed a meta-analysis across 34 datasets of European-ancestry subjects, including 38,617 smokers who were assessed for cigarettes-per-day, 7,700 lung cancer cases and 5,914 lung-cancer-free controls (all smokers), and 2,614 COPD cases and 3,568 COPD-free controls (all smokers). We demonstrate statistically independent associations of rs16969968 and rs588765 with smoking (mutually adjusted p-values<10$^{−35}$ and <10$^{−8}$ respectively). Because the risk alleles at these loci are negatively correlated, their association with smoking is stronger in the joint model than when each SNP is analyzed alone. Rs578776 also demonstrates association with smoking after adjustment for rs16969968 (p<10$^{−6}$). In models adjusting for cigarettes-per-day, we confirm the association between rs16969968 and lung cancer (p<10$^{−20}$) and observe a nominally significant association with COPD (p = 0.01); the other loci are not significantly associated with either lung cancer or COPD after adjusting for rs16969968. This study provides strong evidence that multiple statistically distinct loci in this region affect smoking behavior. This study is also the first report of association between rs588765 (and correlates) and smoking that achieves genome-wide significance; these SNPs have previously been associated with mRNA levels of CHRNA5 in brain and lung tissue

Severe Osteogenesis Imperfecta in Cyclophilin B–Deficient Mice

Osteogenesis Imperfecta (OI) is a human syndrome characterized by exquisitely fragile bones due to osteoporosis. The majority of autosomal dominant OI cases result from point or splice site mutations in the type I collagen genes, which are thought to lead to aberrant osteoid within developing bones. OI also occurs in humans with homozygous mutations in Prolyl-3-Hydroxylase-1 (LEPRE1). Although P3H1 is known to hydroxylate a single residue (pro-986) in type I collagen chains, it is unclear how this modification acts to facilitate collagen fibril formation. P3H1 exists in a complex with CRTAP and the peptidyl-prolyl isomerase cyclophilin B (CypB), encoded by the Ppib gene. Mutations in CRTAP cause OI in mice and humans, through an unknown mechanism, while the role of CypB in this complex has been a complete mystery. To study the role of mammalian CypB, we generated mice lacking this protein. Early in life, Ppib-/- mice developed kyphosis and severe osteoporosis. Collagen fibrils in Ppib-/- mice had abnormal morphology, further consistent with an OI phenotype. In vitro studies revealed that in CypB–deficient fibroblasts, procollagen did not localize properly to the golgi. We found that levels of P3H1 were substantially reduced in Ppib-/- cells, while CRTAP was unaffected by loss of CypB. Conversely, knockdown of either P3H1 or CRTAP did not affect cellular levels of CypB, but prevented its interaction with collagen in vitro. Furthermore, knockdown of CRTAP also caused depletion of cellular P3H1. Consistent with these changes, post translational prolyl-3-hydroxylation of type I collagen by P3H1 was essentially absent in CypB–deficient cells and tissues from CypB–knockout mice. These data provide significant new mechanistic insight into the pathophysiology of OI and reveal how the members of the P3H1/CRTAP/CypB complex interact to direct proper formation of collagen and bone