Property Agents and Motor Dealers Act : strike three

The Tourism, Racing and Fair Trading (Miscellaneous Provisions) Act 2002 (“the Act”) which was passed on 18 April 2002 contains a number of significant amendments relevant to the operation of the Property Agents and Motor Dealers Act 2000. The main changes relevant to property transactions are: (i) Changes to the process for appointment of a real estate agent and consolidation of the appointment forms; (ii) Additions to the disclosure obligation of agents and property developers; (iii) Simplification of the process for commencing the cooling off period; (iv) Alteration of the common law position concerning when the parties are bound by a contract; (v) Removal of the requirement for a seller’s signature on the warning statement to be witnessed; (vi) Retrospective amendment of s 170 of the Body Corporate and Community Management Act 1997; (vii) Inclusion of a new power to allow inspectors to enter the place of business of a licensee or a marketeer without consent and without a warrant; and (viii) Inclusion of a new power for inspectors to require documents to be produced by marketeers. The majority of the amendments are effective from the date of assent, 24 April 2002, however, some of the amendments do not commence until a date fixed by proclamation. No proclamation has been made at the time of writing (2 May 2002). Where the amendments have not commenced this will be noted in the article. Before providing clients with advice, practitioners should carefully check proclamation details.

Black v Garnock : implications for Queensland conveyancing practice

What was previously established as a fundamental principle, that a judgment creditor may take no interest beyond what the judgment debtor could give, has now been called into question by the decision of the High Court in Black v Garnock [2007] HCA 31. This article examines the implications of the decision of the High Court for conveyancing practice in Queensland. The relevant facts of Black v Garnock [2007] HCA 31 may be briefly stated: The Garnocks and the Luffs, as purchasers, entered a contract to purchase a rural property from Mrs Smith with settlement due on 24 August 2005. On 23 August 2005, a creditor obtained a writ against Mrs Smith from the District Court of New South Wales. No caveat was lodged on behalf of the purchasers prior to settlement (there being no equivalent, in New South Wales, of the Queensland settlement notice mechanism).

Exposure to particles from laser printers operating within office workplaces

While recent research has provided valuable information as to the composition of laser printer particles, their formation mechanisms, and explained why some printers are emitters whilst others are low emitters, fundamental questions relating to the potential exposure of office workers remained unanswered. In particular, (i) what impact does the operation of laser printers have on the background particle number concentration (PNC) of an office environment over the duration of a typical working day?; (ii) what is the airborne particle exposure to office workers in the vicinity of laser printers; (iii) what influence does the office ventilation have upon the transport and concentration of particles?; (iv) is there a need to control the generation of, and/or transport of particles arising from the operation of laser printers within an office environment?; (v) what instrumentation and methodology is relevant for characterising such particles within an office location? We present experimental evidence on printer temporal and spatial PNC during the operation of 107 laser printers within open plan offices of five buildings. We show for the first time that the eight-hour time-weighted average printer particle exposure is significantly less than the eight-hour time-weighted local background particle exposure, but that peak printer particle exposure can be greater than two orders of magnitude higher than local background particle exposure. The particle size range is predominantly ultrafine (< 100nm diameter). In addition we have established that office workers are constantly exposed to non-printer derived particle concentrations, with up to an order of magnitude difference in such exposure amongst offices, and propose that such exposure be controlled along with exposure to printer derived particles. We also propose, for the first time, that peak particle reference values be calculated for each office area analogous to the criteria used in Australia and elsewhere for evaluating exposure excursion above occupational hazardous chemical exposure standards. A universal peak particle reference value of 2.0 x 104 particles cm-3 has been proposed.

The factor V HR2 haplotype: Prevalence and association of the A4070G and A6755G polymorphisms

Recently, a polymorphism was identified in exon 25 of the factor V gene that is possibly a functional candidate for the HR2 haplotype. This haplotype is characterized by a single base substitution named R2 (A4070G) in the B domain of the protein. A mutation (A6755G; 2194Asp→Gly) located near the C terminus has been hypothesized to influence protein folding and glycosylation, and might be responsible for the shift in factor V isoform (FV1 / FV2) ratio. This study investigated the prevalence of these two factor V HR2 haplotype polymorphisms in a cohort of normal blood donors, patients with osteoarthritis and women with complications during pregnancy, and in families of factor V Leiden individuals. A high allele frequency for the two polymorphisms was found in the blood donor group (6.2% R2, 5.6% A6755G). No significant difference in allele frequency was observed in the clinical groups (obstetric complications and osteoarthritis, 4.1-4.9% for the two polymorphisms) when compared with that of healthy blood donors. We confirm that the factor V A6755G polymorphism shows strong linkage to the R2 allele, although it is not exclusively inherited with the exon 13 A4070G variant and can occur independently. © 2001 Lippincott Williams & Wilkins.

Use of first nucleotide change technology to determine the frequency of factor V Leiden in a population of Australian blood donors

Activated protein C resistance (APCR), the most common risk factor for venous thrombosis, is the result of a G to A base substitution at nucleotide 1691 (R506Q) in the factor V gene. Current techniques to detect the factor V Leiden mutation, such as determination of restriction length polymorphisms, do not have the capacity to screen large numbers of samples in a rapid, cost- effective test. The aim of this study was to apply the first nucleotide change (FNC) technology, to the detection of the factor V Leiden mutation. After preliminary amplification of genomic DNA by polymerase chain reaction (PCR), an allele-specific primer was hybridised to the PCR product and extended using fluorescent terminating dideoxynucleotides which were detected by colorimetric assay. Using this ELISA-based assay, the prevalence of the factor V Leiden mutation was determined in an Australian blood donor population (n = 500). A total of 18 heterozygotes were identified (3.6%) and all of these were confirmed with conventional MnlI restriction digest. No homozygotes for the variant allele were detected. We conclude from this study that the frequency of 3.6% is compatible with others published for Caucasian populations. In addition, the FNC technology shows promise as the basis for a rapid, automated DNA based test for factor V Leiden.

Evidence for u.v. induction of CDKN2 mutations in melanoma cell lines

The CDKN2 gene, encoding the cyclin dependent kinase inhibitor p16, is a tumour suppressor gene involved in melanoma and maps to chromosome band 9p22. Mutations or interstitial deletions of this gene have been found both in the germline of familial melanoma cases and somatically in melanoma cell lines. Previous mutation analyses of melanoma cell lines have indicated a high frequency of C:G to T:A transitions, with all of these mutations occurring at dipyrimidine sites. Including three melanoma cell lines carrying tandem CC to TT mutations, the spectrum of mutations so far reported indicates a possible role for u.v. radiation in the mutagenesis of this gene in some tumours. To further examine this hypothesis we have characterised mutations of the CDKN2 gene in 30 melanoma cell lines. Nineteen lines carried complete or partial homozygous deletions of the gene. Of the remaining cell lines, eight were shown by direct sequencing of PCR products from exon 1 and exon 2 to carry a total of nine different mutations of CDKN2. Two cell lines carried tandem CC to TT mutations and a high rate of C:G to T:A transitions was observed. This study provides further evidence for the role of u.v. light in the genesis of melanoma, with one target being the CDKN2 tumour suppressor gene.