Faster clonal turnover in high-infection habitats provides evidence for parasite-mediated selection.

According to the Red Queen hypothesis for sex, parasite-mediated selection against common clones counterbalances the reproductive advantage of asexual lineages, which would otherwise outcompete sexual conspecifics. Such selection on the clonal population is expected to lead to a faster clonal turnover in habitats where selection by parasites is stronger. We tested this prediction by comparing the genetic structure of clonal and sexual populations of freshwater snail Potamopyrgus antipodarum between years 2003 and 2007 in three depth-specific habitats in Lake Alexandrina (South Island, New Zealand). These habitats differ in the risk of infection by castrating trematodes and in the relative proportion of sexual individuals. As predicted, we found that the clonal structure changed significantly in shallow and mid-water habitats, where prevalence of infection was high, but not in the deep habitat, where parasite prevalence was low. Additionally, we found that both clonal diversity and evenness of the asexual population declined in the shallow habitat. In contrast, the genetic structure (based on F-statistics) of the coexisting sexual population did not change, which suggests that the change in the clonal structure cannot be related to genetic changes in the sexual population. Finally, the frequency of sexuals had no effect on the diversity of the sympatric clonal population. Taken together, our results show a more rapid clonal turnover in high-infection habitats, which gives support for the Red Queen hypothesis for sex.

Exceptional cryptic diversity and multiple origins of parthenogenesis in a freshwater ostracod.

The persistence of asexual reproduction in many taxa depends on a balance between the origin of new asexual lineages and the extinction of old ones. This turnover determines the diversity of extant asexual populations and so influences the interaction between sexual and asexual modes of reproduction. Species with mixed reproduction, like the freshwater ostracod (Crustacea) morphospecies Eucypris virens, are a good model to examine these dynamics. This species is also a geographic parthenogen, in which sexual females and males co-exist with asexual females in the circum-Mediterranean area only, whereas asexual females occur all over Europe. A molecular phylogeny of E. virens based on the mitochondrial COI and 16S fragments is presented. It is characterised by many distinct clusters of haplotypes which are either exclusively sexual or asexual, with only one exception, and are often separated by deep branches. Analysis of the phylogeny reveals an astonishing cryptic diversity, which indicates the existence of a species complex with more than 40 cryptic taxa. We therefore suggest a revision of the single species status of E. virens. The phylogeny indicates multiple transitions from diverse sexual ancestor populations to asexuality. Although many transitions appear to be ancient, we argue that this may be an artefact of the existence of unsampled or extinct sexual lineages.

The spread of apomixis and its effect on resident genetic variation.

In a simulation model we investigated how much of the initial genetic variation that is retained in a population after a dominant mutation has brought apomixis to fixation in it. A marker allele associated with the apomixis mutation is generally retained after the fixation of apomixis, particularly if the two alleles are closely linked. The spread of asexuality, however, normally leads to almost no loss of genetic variation, neither with respect to cytotypes nor with respect to genotypes. This holds for large populations and apomixis mutants with strong pollen production. In smaller populations, and with apomicts with reduced pollen production, the outcome is more variable, ranging from no genetic variation retained to only weakly reduced variability compared with the initial state. These results help explain the high genetic variability in many apomicts. They also imply that natural selection will have many genotypes to act on even after the spread of apomixis.

Inhalation of corticosteroids after hospital care for respiratory syncytial virus infection diminishes development of asthma in infants.

UNLABELLED: The aim of the study was to assess the effect of inhaled corticosteroids on subsequent respiratory symptoms and asthma in infants hospitalized for respiratory syncytial virus infection (RSV). The study included 188 children below 12 mo of age, hospitalized because of RSV infection. During the winter of 1994/95 only selected children (13%) were given inhaled corticosteroids following discharge from the hospital. The following winter (1995/96), almost all children (86%) were given this treatment for 6-8 wk. Outcomes of the two different treatment regimens were compared by questionnaire 19-24 mo after discharge. Children hospitalized and treated during the winter of 1995/96 developed asthma (12% vs. 24%) and other severe symptoms of the respiratory tract less often than infants treated the year before. The frequency of children with less severe symptoms did not differ between the two treatment periods. CONCLUSION: The results indicate that inhalation of corticosteroids for 6-8 wk may reduce subsequent asthma and severe respiratory morbidity in infants hospitalized for RSV infection.

Islet cell surface antibodies are more common in patients and relatives in areas and during seasons with high incidence of insulin-dependent diabetes mellitus.

Although existence of islet cell antibodies (ICA) is regarded as secondary to beta cell death, islet cell surface antibodies (ICSA) might play a role in the disease process. We have collected information from nine European clinics to determine whether ICSA are more common in diabetic children or their relatives in geographical areas or time periods of high incidence of insulin-dependent diabetes mellitus (IDDM). In Finland and Sweden ("North group") with a high incidence of IDDM during childhood, 36% of the patients were positive or weakly positive for ICSA at diagnosis compared with 24% in France (p = 0.1), 11% in Berlin-Vienna (p < 0.01), and 14% in Italy (p < 0.01). This difference was seen in all age groups but was most pronounced in the youngest (0-4 y). This geographical difference was also seen among family members of whom 46% were positive or weakly positive in the North group, 25% in France (p < 0.001), 21% in Berlin-Vienna (p < 0.001), and 16% in Italy (p < 0.001). Of several analyzed antibodies (ICA, gastric parietal cell, thyroglobulin, and thyroid microsomal), only ICSA showed simultaneous positivity in all family members (r = 0.32, p < 0.01). ICSA were most common in family members of patients with short (< 8 d) duration of symptoms (p < 0.05) and showed a similar seasonality, both in patients and relatives, as the incidence of IDDM. We conclude that the geographical difference in incidence of childhood IDDM in Europe may be associated to similar geographical differences in occurrence of ICSA both in newly diagnosed diabetic children and in their relatives. Simultaneous existence of ICSA in both patients and family members and a similar seasonality for ICSA and incidence of IDDM suggest that ICSA may reflect an ongoing disease process.

Indications for a more aggressive disease process in newly diagnosed insulin-dependent diabetic children in northern than in southern Europe.

Finland and Sweden have the highest incidence of insulin-dependent diabetes in children in the world, about 3-4 times that of countries in the Mediterranean area, with the exception of Sardinia. We have collected information from several European clinics and from Pittsburgh, USA, in order to find out whether this difference incidence is associated with corresponding differences of the disease pattern. Patients in Finland or Sweden ('North') and Pittsburgh were younger (< 10 years old) at diagnosis compared with those in the other clinics in Europe (P < 0.05 versus P < 0.02). In the North, boys were in excess (58%) in contrast to France (40%) and Pittsburgh (46%). Patients in the North had a shorter duration of symptoms (< 8 days; P < 0.001) and higher blood glucose (> 20 mmol/l; P < 0.05) than those attending the other European clinics. Irrespective of age, there were more ICA-positive patients in the North (94%) than in Berlin-Vienna (67%; P < 0.01) or in France (70%; P < 0.01). There was a tendency for non-diabetic parents and siblings in the North to have lower C-peptide values (< 0.26 pmol/ml) at the time of diagnosis of the proband and to be ICA-positive more often than relatives in the other European clinics. The seasonal variation of diagnosis showed no obvious geographical differences, with recorded diagnosis always lowest during the summer. We conclude that certain factors seem to cause not only a high incidence of diabetes in children in Finland and Sweden but perhaps also a more aggressive early disease process.

Glycogen synthetase activity in rat muscle in thermal trauma.

The glycogen synthetase activity and glycogen concentration were studied in rat skeletal muscle 24 hours after infliction of a burn. The active I-form of the enzyme was reduced. The total synthetase activity was unchanged. Expressed as a percentage of total synthetase activity, the I-form was decreased from 43.4% in control rats to 27.6% in burned rats. The fasting concentrations of serum insulin and muscle glycogen were not altered by the burn. The reduced synthetase I-form may explain the reduced glycogen storage capacity, demonstrated previously after a similar burn.