Outcomes and indicators, measurement tools, and databases for the National Action Plan for Promotion, Prevention and Early Intervention for Mental Health 2000

This publication is a support and resource document for the "National Action Plan for Promotion, Prevention and Early Intervention for Mental Health 2000". It includes indicators, measurement tools and databases relevant to assessing the implementation of the outcomes and strategies identified in the action plan.

Beyond the middle: A report about literacy and numeracy development of target group students in the middle years of schooling: Volume 2 (Appendices)

This research project was commissioned by the Commonwealth Department of Education, Science and Training to investigate the perceived efficacy of middle years programs in all States and Territories in improving the quality of teaching, learning and student outcomes - especially in literacy and numeracy and for student members of particular target groups. The latter groups included students from lower socio-economic communities, Aboriginal and Torres Strait Islander (Indigenous) communities, students with a Language Background Other than English (hereafter LBOTE), rural and remote students, and students struggling with the transition from middle/upper primary to the junior secondary years.

Conclusions

The researchers focussed on the impact of the heroin shortage that occurred in early 2001 on three Australian jurisdictions, namely NSW, Vic and SA. They interviewed 82 heroin dependent heroin users and 172 key informants from health and law enforcement agencies. They also examined a range of indicator data such as drug seizures, drug-related arrests, deaths related to drug use, emergency department admissions for overdose or drug induced psychosis , calls to telephone help lines about drug use, needles distributed for drug use, and notifications about blood borne diseases. In addition a range of documentation, in particular from the law enforcement sector, was examined.

Cystic fibrosis and CFTR

Cystic fibrosis (CF) is a complex disease affecting epithelial ion transport. There are not many diseases like CF that have triggered such intense research activities. The complexity of the disease is due to mutations in the CFTR protein, now known to be a Cl- channel and a regulator of other transport proteins. The various interactions and the large number of disease-causing CFTR mutations is the reason for a variable genotype-phenotype correlation and sometimes unpredictable clinical manifestation. Nevertheless, the research of the past 10 years has resulted in a tremendous increase in knowledge, not only in regard to CFTR but also in regard to molecular interactions and completely new means of ion channel and gene therapy.

Pharmacotherapy of the ion transport defect in cystic fibrosis

1. More than 1300 different mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) cause cystic fibrosis (CF), a disease characterized by deficient epithelial Cl- secretion and enhanced Na+ absorption. The clinical course of the disease is determined by the progressive lung disease. Thus, novel approaches in pharmacotherapy are based primarily on correction of the ion transport defect in the airways. 2. The current therapeutic strategies try to counteract the deficiency in Cl- secretion and the enhanced Na+ absorption. A number of compounds have been identified, such as genistein and xanthine derivatives, which directly activate mutant CFTR. Other compounds may activate alternative Ca2+-activated Cl- channels or basolateral K+ channels, which supply the driving force for Cl- secretion. Apart from that, Na+ channel blockers, such as phenamil and benzamil, are being explored, which counteract the hyperabsorption of NaCl in CF airways. 3. Clinical trials are under way using purinergic compounds such as the P2Y(2) receptor agonist INS365. Activation of P2Y(2) receptors has been found to both activate Cl- secretion and inhibit Na+ absorption. 4. The ultimate goal is to recover Cl- channel activity of mutant CFTR by either enhancing synthesis and expression of the protein or by activating silent CFTR Cl- channels. Strategies combining these drugs with compounds facilitating Cl- secretion and inhibiting Na+ absorption in vivo may have the best chance to counteract the ion transport defect in cystic fibrosis.