Sulfite : Cytochrome c oxidoreductase from Thiobacillus novellus - Purification, characterization, and molecular biology of a heterodimeric member of the sulfite oxidase family

Direct oxidation of sulfite to sulfate occurs in various photo- and chemotrophic sulfur oxidizing microorganisms as the final step in the oxidation of reduced sulfur compounds and is catalyzed by sulfite:cytochrome c oxidoreductase (EC 1.8.2.1), Here we show that the enzyme from Thiobacillus novellus is a periplasmically located alpha beta heterodimer, consisting of a 40.6-kDa subunit containing a molybdenum cofactor and an 8.8-kDa monoheme cytochrome c(552) smbunit (midpoint redox potential, Em(8.0) = +280 mV), The organic component of the molybdenum cofactor was identified as molybdopterin contained in a 1:1 ratio to the Mo content of the enzyme. Electron paramagnetic resonance spectroscopy revealed the presence of a sulfite-inducible Mo(V) signal characteristic of sulfite:acceptor oxidoreductases. However, pH-dependent changes in the electron paramagnetic resonance signal were not detected. Kinetic studies showed that the enzyme exhibits a ping-pong mechanism involving two reactive sites. K-m values for sulfite and cytochrome c(550) were determined to be 27 and 4 mu M, respectively; the enzyme was found to be reversibly inhibited by sulfate and various buffer ions. The sorAB genes, which encode the enzyme, appear to form an operon, which is preceded by a putative extracytoplasmic function-type promoter and contains a hairpin loop termination structure downstream of sorB. While SorA exhibits significant similarities to known sequences of eukaryotic and bacterial sulfite:acceptor oxidoreductases, SorB does not appear to be closely related to any known c-type cytochromes.

Parent training skills and methadone maintenance: clinical opportunities and challenges

Children raised in substance abusing families show high rates of behavioural and emotional problems, in particular oppositional, defiant and non-compliant behaviours. While a range of social and individual factors correlate with poor parenting, it is often the quality of the parent-child relationship that mediates the effects of most other risk factors on child development. By addressing this relationship using behavioural family interventions, child behaviour problems have been reduced in multiple problem families. However, there has been little attempt to systematically evaluate such programs in substance abusing families. It is argued that methadone replacement programs provide a window of opportunity to deliver well-validated parent training programs that enhance the quality of parent-child relations. However, it is likely that such programs would need to be medium to long term and address issues beyond parent child relationships. How such interventions may be delivered and evaluated is discussed. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.

Discovery and characterization of a family of insecticidal neurotoxins with a rare vicinal disulfide bridge

We have isolated a family of insect-selective neurotoxins from the venom of the Australian funnel-web spider that appear to be good candidates for biopesticide engineering. These peptides, which we have named the Janus-faced atracotoxins (J-ACTXs), each contain 36 or 37 residues, with four disulfide bridges, and they show no homology to any sequences in the protein/DNA databases. The three-dimensional structure of one of these toxins reveals an extremely rare vicinal disulfide bridge that we demonstrate to be critical for insecticidal activity. We propose that J-ACTX comprises an ancestral protein fold that we refer to as the disulfide-directed beta-hairpin.

Relationships among climate, latitude and migration: Australian butterflies are not temperate-zone birds

We examined the distribution of butterflies over the mostly arid and semi-arid continent of Australia and analyzed the proportion of migrant species and species diversity with respect to an array of climatic and geographic variables. On a continent-wide scale, latitude explained virtually no variance in either proportion of migrants (r(2) = 0.01) or species diversity (r(2) = 0.03) in Australian butterflies. These results are in marked contrast to those for temperate-zone birds from three continents where latitude explained between 82 and 98% of the variance in frequency of migrants and also accounted for much of the variance in bird species diversity. In eastern Australia where rainfall regimes are similar to those in temperate Europe and North and South America, latitude explains 78% of the variance in frequency of butterfly migrants. In both eastern and central Australia, latitude also accounts for relatively high proportions of the variance in species diversity. Rainfall patterns and especially soil moisture are negatively associated with migration frequency in Australian butterfly faunas, both alone and in combination with other climate variables. Where moisture levels are relatively high, as in eastern Australia, measures of temperature are associated with migration frequency, a result consistent with findings for temperate-zone birds, suggesting latitude is a surrogate for temperature. The ultimate causes of migration in temperate-zone birds and Australian butterflies are the uneven temporal, and in Australia also spatial, distribution of resources. Uneven distribution is brought about primarily by temperature in temperate regions and by erratic rainfall over much of arid Australia. As a key determinant of productivity, especially in the tropics and subtropics, aridity is likely to be an important determinant of the global distributions of migrants.

Absolute risk of breast cancer for Australian women with a family history

Background: The purpose of the present paper was to estimate the absolute risk of breast cancer over the remainder of a lifetime in Australian women with different categories of family history. Methods: Age-specific breast cancer incidence rates were adjusted for screening effects, and rates in those with no family history were estimated using the attributable fraction (AF). Relative risks from a published meta-analysis were applied to obtain incidence rates for different categories of family history, and age-specific incidence was converted to cumulative risk of breast cancer. The risk estimates were based upon Australian population statistics and published relative risks. Breast cancer incidence was from New South Wales women for 1996. The AF was calculated using prevalence of a family history of breast cancer from data on Queensland women. The cumulative absolute risk of breast cancer was calculated from decade and mid-decade ages to age 79 years, not adjusted for competing causes of death. Results: Lifetime risk is approximately 8.6% (1 in 12) for the general population and 7.8% (1 in 13) for those without a family history. Women with one relative affected have lifetime risks of 1 in 6-8 and those with two relatives affected have lifetime risks of 1 in 4-6. The cumulative residual lifetime risk decreases with advancing age; by age 60 years all groups with only one relative affected have well above a 90% probability of not developing breast cancer to age 79 years. Conclusions: These Australian risk statistics are useful for public information and in the clinical setting. Risks given here apply to women with average breast cancer risk from other risk factors.

Relationships between body mass index and well-being in young Australian women

OBJECTIVE: To explore relationships between body mass index (BMI, kg/m(2)) and indicators of health and well-being in young Australian women. DESIGN: Population based cohort study-baseline cross sectional data. SUBJECTS: 14,779 women aged 18-23 who participated in the baseline survey of the Australian Longitudinal Study on Women's Health in 1996. MEASUREMENTS: Self-reported height, weight, medical conditions, symptoms and SF-36. RESULTS: The majority of women (68%) had a BMI in the range 18.5-

Predictors of genital warts among women attending two family planning clinics

Objectives: To establish the prevalence and predictors of genital warts among healthy women presenting for contraceptive advice at two family planning clinics, one in a major Australian city and one in a country town in the same state. Methods: Consecutive consenting attendees (n = 1218)at two family planning clinics in Queensland completed a questionnaire and were examined for genital warts. Results: The point prevalence of visible genital warts was 3.3 per cent in the city clinic and 14.4 per cent in the country town. For half of these clients a finding of warts was unexpected, in that the client was unaware of their presence and presentation to the family planning clinic was not specifically for advice about sexually transmitted infections. The major predictor of a finding of warts was client age, with the highest prevalence in 20- to 25-year-olds. Warts were also commoner amongst smokers in the country town but not in Brisbane. However, no analysed sociodemographic variable predicted a finding of warts of which the client was not aware. Conclusions: Genital warts are common among young women presenting for contraceptive advice. Such women are often unaware that they have warts. Examination for genital warts should be a part of any routine examination of sexually active women, and medical practitioners should be aware of appropriate advice for patients who are found to have genital warts on routine examination.

Truncation of the GABA(A)-receptor gamma 2 subunit in a family with generalized epilepsy with febrile seizures plus

Recent findings from studies of two families have shown that mutations in the GABA(A)-receptor gamma2 subunit are associated with generalized epilepsies and febrile seizures. Here we describe a family that has generalized epilepsy with febrile seizures plus (GEFS(+)), including an individual with severe myoclonic epilepsy of infancy, in whom a third GABA(A)-receptor gamma2-subunit mutation was found. This mutation lies in the intracellular loop between the third and fourth transmembrane domains of the GABA(A)-receptor gamma2 subunit and introduces a premature stop codon at Q351 in the mature protein. GABA sensitivity in Xenopus laevis oocytes expressing the mutant gamma2(Q351X) subunit is completely abolished, and fluorescent-microscopy studies have shown that receptors containing GFP-labeled gamma2(Q351X) protein are retained in the lumen of the endoplasmic reticulum. This finding reinforces the involvement of GABA(A) receptors in epilepsy.

A family of perfect factorisations of complete bipartite graphs

A 1-factorisation of a graph is perfect if the union of any two of its 1-factors is a Hamiltonian cycle. Let n = p(2) for an odd prime p. We construct a family of (p-1)/2 non-isomorphic perfect 1-factorisations of K-n,K-n. Equivalently, we construct pan-Hamiltonian Latin squares of order n. A Latin square is pan-Hamiltoilian if the permutation defined by any row relative to any other row is a single Cycle. (C) 2002 Elsevier Science (USA).

Childhood absence epilepsy and febrile seizures: A family with a GABAA receptor mutation

Although several genes for idiopathic epilepsies from families with simple Mendelian inheritance have been found, genes for the common idiopathic generalized epilepsies, where inheritance is complex, presently are elusive. We studied a large family with epilepsy where the two main phenotypes were childhood absence epilepsy (CAE) and febrile seizures (FS), which offered a special opportunity to identify epilepsy genes. A total of 35 family members had seizures over four generations. The phenotypes comprised typical CAE (eight individuals); FS alone (15), febrile seizures plus (FS+) (three); myoclonic astatic epilepsy (two); generalized epilepsy with tonic-clonic seizures alone (one); partial epilepsy (one); and unclassified epilepsy despite evaluation (two). In three remaining individuals, no information was available. FS were inherited in an autosomal dominant fashion with 75% penetrance. The inheritance of CAE in this family was not simple Mendelian, but suggestive of complex inheritance with the involvement of at least two genes. A GABA(A) receptor gamma2 subunit gene mutation on chromosome 5 segregated with FS, FS+ and CAE, and also occurred in individuals with the other phenotypes. The clinical and molecular data suggest that the GABA(A) receptor subunit mutation alone can account for the FS phenotype. An interaction of this gene with another gene or genes is required for the CAE phenotype in this family. Linkage analysis for a putative second gene contributing to the CAE phenotype suggested possible loci on chromosomes 10, 13, 14 and 15. Examination of these loci in other absence pedigrees is warranted.