Large-brained birds suffer less oxidative damage.

Large brains (relative to body size) might confer fitness benefits to animals. Although the putative costs of well-developed brains can constrain the majority of species to modest brain sizes, these costs are still poorly understood. Given that the neural tissue is energetically expensive and demands antioxidants, one potential cost of developing and maintaining large brains is increased oxidative stress ('oxidation exposure' hypothesis). Alternatively, because large-brained species exhibit slow-paced life histories, they are expected to invest more into self-maintenance such as an efficacious antioxidative defence machinery ('oxidation avoidance' hypothesis). We predict decreased antioxidant levels and/or increased oxidative damage in large-brained species in case of oxidation exposure, and the contrary in case of oxidation avoidance. We address these contrasting hypotheses for the first time by means of a phylogenetic comparative approach based on an unprecedented data set of four redox state markers from 85 European bird species. Large-brained birds suffered less oxidative damage to lipids (measured as malondialdehyde levels) and exhibited higher total nonenzymatic antioxidant capacity than small-brained birds, whereas uric acid and glutathione levels were independent of brain size. These results were not altered by potentially confounding variables and did not depend on how relative brain size was quantified. Our findings partially support the 'oxidation avoidance' hypothesis and provide a physiological explanation for the linkage of large brains with slow-paced life histories: reduced oxidative stress of large-brained birds can secure brain functionality and healthy life span, which are integral to their lifetime fitness and slow-paced life history.

Road traffic and landscape characteristics predict the occurrence of native halophytes on roadside verges.

Road management practices, such as winter de-icing create ideal habitats and competitive advantage for salt-tolerant species. We aimed to map the occurrences of halophytes along roads in Hungary. Furthermore, we tested factors that might play a role in the roadside occurrences of five chosen native halophytes from rare to common, we encountered during our field surveys. These were Festuca pseudovina, Limonium gmelinii subsp. hungaricum, Podospermum canum, Puccinellia distans and Spergularia media. We found, that at least one halophyte species was documented in 71% of the total sampling points. Germination experiments indicated that substrate salt concentration significantly decreased germination rates in each of the five species, but in case of L. gmelinii subsp. hungaricum, or P. distans germination occurred on extremely high salt concentrations. Traffic intensity, the presence of other halophytes at the sampling point and the presence of a given species in the surrounding landscape had a significant positive effect on the occurrence of four of the five model species. Our results suggest that the studied species are mostly in the early stage of their roadside spread, colonizing roadsides close to their native distribution ranges. The possibility of a future range expansion along roads cannot be excluded.

TPPP/p25: from unfolded protein to misfolding disease: prediction and experiments.

TPPP/p25, the first representative of a new protein family, identified as a brain-specific unfolded protein induces aberrant microtubule assemblies in vitro, suppresses mitosis in Drosophila embryo and is accumulated in inclusion bodies of human pathological brain tissues. In this paper, we present prediction and additional experimental data that validate TPPP/p25 to be a new member of the "intrinsically unstructured" protein family. The comparison of these characteristics with that of alpha-synuclein and tau, involved also in neurodegenerative diseases, suggested that although the primary sequences of these proteins are entirely different, there are similarities in their well-defined unstructured segments interrupted by "stabilization centres", phosphorylation and tubulin binding motives. SK-N-MC neuroblastoma cells were transfected with pEGFP-TPPP/p25 construct and a stable clone denoted K4 was selected and used to establish the effect of this unstructured protein on the energy state/metabolism of the cells. Our data by analyzing the mitochondrial membrane polarization by fluorescence microscopy revealed that the high-energy phosphate production in K4 clone is not damaged by the TPPP/p25 expression. Biochemical analysis with cell homogenates provided quantitative data that the ATP level increased 1.5-fold and the activities of hexokinase, glucosephosphate isomerase, phosphofructokinase, triosephosphate isomerase and glyceraldehyde-3-phosphate dehydrogenase were 1.2 to 2.0-fold higher in K4 as compared to the control. Our modelling using these data and rate equations of the individual enzymes suggests that the TPPP/p25 expression stimulates glucose metabolism. At pathological conditions TPPP/p25 is localized in inclusion bodies in multiple system atrophy, it tightly co-localizes with alpha-synuclein, partially with tubulin and not with vimentin. The previous and the present studies obtained with immunohistochemistry with pathological human brain tissues rendered it possible to classify among pathological inclusions on the basis of immunolabelling of TPPP/p25, and suggest this protein to be a potential linkage between Parkinson's and Alzheimer's diseases.

Hyponatremia and sensorineural hearing loss in preterm infants.

In a case-control study the role of hyponatremia in the hearing loss of preterm infants was investigated. One hundred and sixty-four premature infants treated at the neonatal intensive care unit were screened with transient evoked otoacoustic emission (TEAOE). In 32 infants TEAOE results indicated the need for further investigations. Auditory brainstem response was performed and 22 of 32 cases had bilateral hearing impairment (HI). The birth weight and gestational age in the HI group were 1,425 +/- 528 g and 30.4 +/- 3.7 weeks. The matched control group consisted of 25 infants with a mean birth weight and gestational age of 1,410 +/- 280 g and 31.1 +/- 2.1 weeks. Significant differences were found between the HI and control groups: Apgar score (p < 0.05), pH value (p < 0.01) and pO(2) level (p < 0.05) were lower; the total dose of aminoglycosides (p < 0.01), furosemide usage (p < 0.01), the maximum pCO(2) level (p < 0.01), incubator stay (p < 0.05) and hyponatremia (p < 0.01) were higher, and the duration of hyponatremia (p < 0.05) was longer in the HI group. Multivariate logistic regression revealed that aminoglycoside treatment and hyponatremia were the two most significant factors in the development of hearing impairment. These results suggest that hyponatraemia is an additional risk factor for hearing loss in preterm infants.