Factors controlling volatile organic compounds in dwellings in Melbourne, Australia.

This study characterized indoor volatile organic compounds (VOCs) and investigated the effects of the dwelling characteristics, building materials, occupant activities, and environmental conditions on indoor VOC concentrations in 40 dwellings located in Melbourne, Australia, in 2008 and 2009. A total of 97 VOCs were identified. Nine VOCs, n-butane, 2-methylbutane, toluene, formaldehyde, acetaldehyde, d-limonene, ethanol, 2-propanol, and acetic acid, accounted for 68% of the sum of all VOCs. The median indoor concentrations of all VOCs were greater than those measured outdoors. The occupant density was positively associated with indoor VOC concentrations via occupant activities, including respiration and combustion. Terpenes were associated with the use of household cleaning and laundry products. A petroleum-like indoor VOC signature of alkanes and aromatics was associated with the proximity of major roads. The indoor VOC concentrations were negatively correlated (P < 0.05) with ventilation. Levels of VOCs in these Australian dwellings were lower than those from previous studies in North America and Europe, probably due to a combination of an ongoing temporal decrease in indoor VOC concentrations and the leakier nature of Australian dwellings.

The effects of habitat fragmentation on the social kin structure and mating system of the agile antechinus, Antechinus agilis.

Habitat fragmentation is one of the major contributors to the loss of biodiversity worldwide. However, relatively little is known about its more immediate impacts on within-patch population processes such as social structure and mating systems, whose alteration may play an important role in extinction risk. We investigated the impacts of habitat fragmentation due to the establishment of an exotic softwood plantation on the social kin structure and breeding system of the Australian marsupial carnivore, Antechinus agilis. Restricted dispersal by males in fragmented habitat resulted in elevated relatedness among potential mates in populations in fragments, potentially increasing the risk of inbreeding. Antechinus agilis nests communally in tree hollows; these nests are important points for social contact between males and females in the mating season. In response to elevated relatedness among potential mates in fragmented habitat, A. agilis significantly avoided sharing nests with opposite-sex relatives in large fragment sites (but not in small ones, possibly due to limited nest locations and small population sizes). Because opposite-sex individuals shared nests randomly with respect to relatedness in unfragmented habitat, we interpreted the phenomenon in fragmented habitat as a precursor to inbreeding avoidance via mate choice. Despite evidence that female A. agilis at high inbreeding risk selected relatively unrelated mates, there was no overall increased avoidance of related mates by females in fragmented habitats compared to unfragmented habitats. Simulations indicated that only dispersal, and not nonrandom mating, contributed to inbreeding avoidance in either habitat context. However, habitat fragmentation did influence the mating system in that the degree of multiple paternity was reduced due to the reduction in population sizes and population connectivity. This, in turn, reduced the number of males available to females in the breeding season. This suggests that in addition to the obvious impacts of reduced recruitment, patch recolonization and increased genetic drift, the isolation of populations in habitat patches may cause changes in breeding behaviour that contribute to the negative impacts of habitat fragmentation.

Cell death of spinal interneurones.

The occurrence of neuronal death during development is well documented for some neuronal populations, such as motoneurones and dorsal root ganglion cells, whose connecting pathways are clearly defined. Cell survival is thought to be regulated largely by target and input connections, a process that serves to match the size of synaptically linked neuronal populations. Far less is known about interneurones. It is assumed that most interneurone populations are excluded from this process because their connections are more diffuse. Recent studies on the rat spinal cord have indicated that interneurone death does occur, both naturally during development and induced following peripheral nerve injury. Here the evidence for spinal interneurone death is reviewed and the factors influencing it are discussed. There are many functional types of interneurones in the spinal cord that may differ in vulnerability to cell death, but it is concluded that for most spinal interneurones the traditional view of target regulation is unlikely. Instead it is proposed that developmental interneurone death in the spinal cord forms part of a plastic response to altered sensory activation rather than a size-matching exercise. There is also emerging evidence that interneurone death may play a more direct role in some neurodegenerative diseases than hitherto considered.

Human Nedd4 interacts with the human epithelial Na+ channel: WW3 but not WW1 binds to Na+-channel subunits.

The epithelial Na(+) channel (ENaC) regulates Na(+) absorption in epithelial tissues including the lung, colon and sweat gland, and in the distal nephrons of the kidney. When Na(+)-channel function is disrupted, salt and water homoeostasis is affected. The cytoplasmic regions of the Na(+)-channel subunits provide binding sites for other proteins to interact with and potentially regulate Na(+)-channel activity. Previously we showed that a proline-rich region of the alpha subunit of the Na(+) channel bound to a protein of 116 kDa from human lung cells. Here we report the identification of this protein as human Nedd4, a ubiquitin-protein ligase that binds to the Na(+)-channel subunits via its WW domains. Further, we show that WW domains 2, 3 and 4 of human Nedd4 bind to the alpha, beta and gamma Na(+)-channel subunits but not to a mutated beta subunit. In addition, when co-expressed in Xenopus oocytes, human Nedd4 down-regulates Na(+)-channel activity.

The role of apoptosis and excitotoxicity in the death of spinal motoneurons and interneurons after neonatal nerve injury.

There is evidence that motoneurons which die following neonatal nerve injury in rats do so through an excitotoxic mechanism. In this study, we have investigated whether this excitotoxicity induces motoneuron death by apoptosis. Sciatic motoneurons were prelabelled at birth with the retrograde tracing agent, Fast Blue, and the sciatic nerve was crushed in one leg two days later. At intervals up to 12 days, sections of the lumbar enlargement were analysed for apoptosis using propidium iodide and terminal deoxynucleotidyl transferase biotin-14-UTP nick end labelling techniques. A significant concentration of Fast Blue-labelled apoptotic motoneurons was seen in the area of the sciatic motor pool ipsilateral to the nerve injury, with the majority occurring in the first three days. Comparison of estimates of the time-course of apoptosis with that of motoneuron survival suggest that all motoneuron death induced during the first 12 days occurs by apoptosis and that the process is only recognizable for 2 h. Treatment with the N-methyl-D-aspartate receptor antagonist, dizocilpine maleate, reduced the level of apoptosis by 60%. Taken together, these data show that motoneurons which have been affected by an excitotoxic mechanism die by apoptosis. The apoptotic study also provides evidence, for the first time, that unilateral nerve injury induces motoneuron death in the contralateral sciatic motor pool. Apoptotic interneurons were also seen on both sides of the spinal cord as a result of nerve injury.

Evidence that spinal interneurons undergo programmed cell death postnatally in the rat.

Programmed cell death has been demonstrated in several specific neuronal populations as a mechanism for modulating the population size following differentiation, but its applicability to all neuronal types is unclear. Evidence for programmed cell death in some populations such as the numerous spinal interneurons has been lacking. We have studied the incidence of apoptosis in the rat spinal cord with three different methods and found a previously undocumented wave of apoptosis occurring in spinal grey matter shortly after birth. The apoptotic morphology was confirmed ultrastructurally. Dying cells were identified as neurons by immunocytochemical labelling for neuronal markers and had an anatomical distribution which indicated that most of the apoptotic cells were interneurons not motoneurons. This wave of apoptosis has the characteristics of a discrete developmental process and occurs later than that of either ventral horn motoneurons or dorsal root ganglion cells, to which most spinal interneurons are connected. These findings indicate that interneurons do undergo programmed cell death, and we suggest that this occurs in response to the earlier reduction in size of their main synaptic targets.