Pulsed resources at tundra breeding sites affect winter irruptions at temperate latitudes of a top predator, the snowy owl.

Irruptive migration is mostly observed in species specialized on pulsed resources and is thought to be a response to unpredictable changes in food supply. We assessed two alternative hypotheses to explain the periodic winter irruptions of snowy owls Bubo scandiacus every 3-5 years in temperate North America: (a) the lack-of-food hypothesis, which states that a crash in small mammal abundance on the Arctic breeding grounds forces owls to move out of the tundra massively to search for food in winter; (b) the breeding-success hypothesis, which states that high abundance of tundra small mammals during the summer allows for high production of young, thus increasing the pool of migrants moving south the following winter. We modeled winter irruptions of snowy owls in relation to summer food resources and geographic location. Winter abundance of owls was obtained from citizen-based surveys from 1994 to 2011 and summer abundance of small mammals was collected in summer at two distant sites in Canada: Bylot Island, NU (eastern High Arctic) and Daring Lake, NWT (central Low Arctic). Winter owl abundance was positively related to prey abundance during the previous summer at both sites and tended to decrease from western to eastern temperate North America. Irruptive migration of snowy owls was therefore best explained by the breeding success hypothesis and was apparently caused by large-scale summer variations in food. Our results, combined with previous findings, suggest that the main determinants of irruptive migration may be species specific even in a guild of apparently similar species.

SCID mice containing muscle with human mitochondrial DNA mutations. An animal model for mitochondrial DNA defects.

Defects of the mitochondrial genome are important causes of disease. Despite major advances in our investigation of patients, there is no effective therapy. Progress in this area is limited by the absence of any animal models in which we can evaluate treatment. To develop such a model we have injected human myoblasts into the tibialis anterior of SCID mice after inducing necrosis. After injection of normal human myoblasts, regenerating fibers expressed human beta-spectrin, confirming they were derived from fusion of human myoblasts. The stability of the muscle fibers was inferred by demonstrating the formation of motor end plates on the regenerating fibers. In addition, we show the presence of human cytochrome c oxidase subunit II, which is encoded by the mitochondrial genome, in the regenerated fibers. After injection of human myoblasts containing either the A8344G or the T8993C heteroplasmic mitochondrial DNA mutations, human beta-spectrin positive fibers were found to contain the mutation at a similar level to the injected myoblasts. These studies highlight the potential value of this model for the study of mitochondrial DNA defects.

Neither compatible nor self-incompatible pollinations of Brassica napus involve reorganization of the papillar cytoskeleton.

Compatible pollination of Brassica napus necessitates pollen hydration, pollen germination and growth of the pollen tube through the loosened walls of stigmatic papillar cells, whereas self-incompatible (SI) pollinations fail at one of these stages. Analyses of the early stages of pollination show that at high (but not low) relative humidities, both compatible and SI pollen hydrates, but SI germination is reduced and the rare pollen tubes generally fail to penetrate the papillar walls, although there is some wall loosening. Inside the papillae, both compatible and SI interactions may induce the formation of callose, but there is no evidence for a major accumulation of cytoplasm or secretory vesicles in the vicinity of the pollen tubes and neither microtubule nor F-actin patterns re-arrange in this zone. These observations indicate that the source of the wall-loosening enzymes is probably the pollen tube or pollen coat, and that the common cellular responses of plants to attempted invasions have become suppressed in the papilla-pollen tube interaction.

A longitudinal study of religiosity and mortality risk.

The relation of adult religiosity to longevity was studied in 993 participants from Terman's 70-year Life-Cycle Study. Key social and behavioral variables of physical health, psychological well-being, socioeconomic status, social support, and health behaviors were also considered. Results indicate that women who viewed themselves as more religious in adulthood (approximately age 40) had a lower risk for premature mortality than those who were less religiously inclined. These women had healthier behaviors, more positive feelings about their futures, and reported being somewhat happier than their less religiously inclined peers. In this bright, middle-class, 20th century sample, religiosity among women seems to be part of a generally healthy lifestyle, but not necessarily a direct cause of it.

A comparison of serological tests and gross lung pathology for detecting contagious bovine pleuropneumonia in two groups of Italian cattle.

Western and dot blotting techniques were compared with complement fixation tests (CFT), indirect enzyme-linked immunosorbent assays (ELISA), mycoplasma culture and gross lung pathology to detect Mycoplasma mycoides subspecies mycoides SC, the cause of contagious bovine pleuropneumonia (CBPP), in two groups of Italian cattle. None of the animals showed any clinical signs before slaughter. In group A, seven of the 20 cattle had characteristic lung lesions of acute and chronic CBPP but only six were positive by CFT. Western blotting detected antibody in eight of the animals, of which six had lesions and significant CFT titres (> 50 per cent fixation at a serum dilution of 1/10) and two had neither. In group B, seven of the 17 cattle had lesions characteristic of CBPP, and 12 were seropositive by CFT. Western blotting detected antibody in 13 of the animals including one which had a negative CFT titre. The ELISA was less sensitive than either CFT or Western blotting, detecting antibody in five animals in group A and nine animals in group B. The dot blotting test correlated well with Western blotting but gave a small number of ambiguous results. The causative organism was isolated from four of the 20 cattle in group A and six of the 17 cattle in group B.

Effect of captivity on genetic variance for five traits in the large milkweed bug (Oncopeltus fasciatus).

Understanding the changes in genetic variance which may occur as populations move from nature into captivity has been considered important when populations in captivity are used as models of wild ones. However, the inherent significance of these changes has not previously been appreciated in a conservation context: are the methods aimed at founding captive populations with gene diversity representative of natural populations likely also to capture representative quantitative genetic variation? Here, I investigate changes in heritability and a less traditional measure, evolvability, between nature and captivity for the large milkweed bug, Oncopeltus fasciatus, to address this question. Founders were collected from a 100-km transect across the north-eastern US, and five traits (wing colour, pronotum colour, wing length, early fecundity and later fecundity) were recorded for founders and for their offspring during two generations in captivity. Analyses reveal significant heritable variation for some life history and morphological traits in both environments, with comparable absolute levels of evolvability across all traits (0-30%). Randomization tests show that while changes in heritability and total phenotypic variance were highly variable, additive genetic variance and evolvability remained stable across the environmental transition in the three morphological traits (changing 1-2% or less), while they declined significantly in the two life-history traits (5-8%). Although it is unclear whether the declines were due to selection or gene-by-environment interactions (or both), such declines do not appear inevitable: captive populations with small numbers of founders may contain substantial amounts of the evolvability found in nature, at least for some traits.

Treatment of mitochondrial disease.

Defects of the mitochondrial genome are widely recognized as important causes of disease in man. Patients may present at any age with clinical symptoms that vary from acute episodes of lactic acidosis in infancy to severe neurodegenerative illness in adulthood. While modern molecular genetic techniques have facilitated major advances in the diagnosis and characterization of specific molecular defects, treatment for the majority of patients remains supportive in the absence of definitive biochemical therapies. As a consequence, the possibilities for mitochondrial DNA gene therapy must be considered. In this review, we will evaluate the current biochemical strategies available to clinicians for the management of patients with mitochondrial disease and examine the possible approaches to the gene therapy of mitochondrial DNA defects.

Immunological functions of aged human monocytes.

Aging is associated with an increased occurrence of infection and cancer, and, as people age, they begin to exhibit age-related immune deficiencies, collectively termed immunosenescence. To determine the effects of age on human monocytes, 'aged monocytes' (isolated from individuals > or = 65 years of age) were compared with 'young monocytes' (isolated from individuals approximately 25 years of age) for their ability to be activated by lipopolysaccharide. Our results show that aged monocytes display a decrease in their cytotoxicity against tumor cells in vitro, a decrease in interleukin (IL1) secretion (although no decrease in IL1 precursor production was observed), a decrease in reactive oxygen and nitrogen intermediate (ROI/RNI) release, an increase in intracellular levels of cyclic adenosine monophosphate and a loss of protein kinase translocation. Therefore, aged monocytes present distinct characteristics of immunosenescence.

Raciation and speciation in house mice from the Alps: the role of chromosomes.

There are at least 24 different karyotypic races of house mouse in the central Alps, each characterized by a different complement of ancestral acrocentric and derived metacentric chromosomes; altogether 55 different metacentric chromosomes have been described from the region. We argue that this chromosome variation largely arose in situ. If these races were to make contact, in most cases they would produce F1 hybrids with substantial infertility (sometimes complete sterility), due to nondisjunction and germ cell death associated with the formation of long-chain and/or ring configurations at meiosis. We present fertility estimates to confirm this for two particular hybrid types, one of which demonstrates male-limited sterility (in accordance with Haldane's Rule). As well as a model for speciation in allopatry, the Alpine mouse populations are of interest with regards speciation in parapatry: we discuss a possible reinforcement event. Raciation of house mice appears to have happened on numerous occasions within the central Alps. To investigate one possible source of new karyotypic races, we use a two-dimensional stepping stone model to examine the generation of recombinant races within chromosomal hybrid zones. Using field-derived ecological data and laboratory-derived fertility estimates, we show that hybrid karyotypic races can be generated at a reasonable frequency in simulations. Our model complements others developed for flowering plants that also emphasize the potential of chromosomal hybrid zones in generating new stable karyotypic forms.

Recurrent herpes simplex virus labialis and the use of epidural morphine in obstetric patients.

A retrospective study of sequential obstetric patients delivering at University Hospital and receiving epidural anesthesia was conducted to determine if a suggested association exists between the recurrence of oral herpes simplex lesions and the use of epidural morphine. In a retrospective study of 291 patients, 13 of 134 (9.7%) receiving epidural morphine developed recurrent oral herpes lesions in contrast to 1 of 157 (0.6%) not receiving the drug (P less than 0.001). In a prospective hospital-based study of 729 consecutive obstetric patients, 146 patients received epidural opioids (morphine, fentanyl, or both) and 583 did not. Recurrent HSVL lesions occurred in 13 of 140 (9.3%) patients given epidural morphine but in only 6 of 583 (1.0%) not given epidural opioids (P less than 0.001). Three of the 13 patients with HSVL received both epidural morphine and fentanyl and 10 received only epidural morphine. Because of the small numbers of patients receiving only fentanyl, no relation between HSVL reactivation and epidural fentanyl could be established. In patients having caesarean sections, the association of recurrent HSVL and the use of epidural morphine was significant (P = 0.04), suggesting cesarean delivery was not a confounder. A hitherto undescribed triggering agent, epidural morphine, appears to be associated with reactivation of HSVL in obstetric patients in the postpartum period.

An mtDNA mutation in the initiation codon of the cytochrome C oxidase subunit II gene results in lower levels of the protein and a mitochondrial encephalomyopathy.

A novel heteroplasmic 7587T-->C mutation in the mitochondrial genome which changes the initiation codon of the gene encoding cytochrome c oxidase subunit II (COX II), was found in a family with mitochondrial disease. This T-->C transition is predicted to change the initiating methionine to threonine. The mutation load was present at 67% in muscle from the index case and at 91% in muscle from the patient's clinically affected son. Muscle biopsy samples revealed isolated COX deficiency and mitochondrial proliferation. Single-muscle-fiber analysis revealed that the 7587C copy was at much higher load in COX-negative fibers than in COX-positive fibers. After microphotometric enzyme analysis, the mutation was shown to cause a decrease in COX activity when the mutant load was >55%-65%. In fibroblasts from one family member, which contained >95% mutated mtDNA, there was no detectable synthesis or any steady-state level of COX II. This new mutation constitutes a new mechanism by which mtDNA mutations can cause disease-defective initiation of translation.