Evolution of postzygotic reproductive isolation in a guild of deceptive orchids

The evolution of reproductive barriers is of central importance for speciation. Here, we investigated three components of postzygotic isolation-embryo mortality, hybrid inviability, and hybrid sterility-in a group of food-deceptive Mediterranean orchids from the genera Anacamptis, Neotinea, and Orchis. In these orchids, pollinator-mediated isolation is weak, which suggests that postpollination barriers exist. Based on crossing experiments and a literature survey, we found that embryo mortality caused complete reproductive isolation among 36.3% of the species pairs, and hybrid inviability affected 55.6% of the potentially hybridizing species pairs. Hybrid sterility was assessed experimentally for seven species pairs. A strong reduction of fertility in all investigated hybrids was found, together with clear differences between male and female components of hybrid sterility. Postzygotic isolation was found to evolve gradually with genetic divergence, and late postzygotic isolation (i.e., hybrid inviability and sterility) evolved faster than embryo mortality, which is an earlier postzygotic isolation stage. These results reveal that intrinsic postzygotic isolation strongly contributes to maintaining species boundaries among Mediterranean food-deceptive orchids while establishing a prominent role for these reproductive barriers in the early stage of species isolation.     

The Search for Meaning: Eventfulness in the Lives of Homeless Mentally Ill Persons in the Skid Row District of Los Angeles

In the past two decades, the field ofpsychiatry has seen the once dominantpsychoanalytic theories overtaken by biologicalexplanations and approaches to severe mentalillness. With this change in perspective, thesignificance of fantasies and delusions havebeen reduced to being merely symptoms ofpsychopathology rather than reflections ofhuman needs and motivations. Usingethnographic evidence from a long-term researchproject, this paper explores one method bywhich mentally ill homeless individuals in theSkid Row district of Los Angeles attempted towrest meaningful lives for themselves out of anenvironment that featured disaffiliation,violence, boredom, and extreme poverty.     

Oligomerization of a Peptide Derived from the Transmembrane Region of the Sodium Pump γ Subunit: Effect of the Pathological Mutation G41R

The Na,K-ATPase, or sodium pump, is a ubiquitously expressed membrane-bound enzyme that controls the transmembrane (TM) gradients of sodium and potassium ions in animal cells. The enzyme comprises two subunits, α and β, and in the kidney, is also associated with a small single-spanning membrane protein, the γ subunit. This 65 amino acid residues protein has been linked to a form of dominant renal hypomagnesaemia resulting from substitution of a highly conserved glycine residue (Gly41) to arginine residue. In order to characterize the quaternary structure of the γ subunit, and effects of the G41R mutation thereupon, we synthesized a series of peptides (wild-type and mutant) that span the γ subunit TM region. Using circular dichroism spectroscopy, we show that the 32-amino acid residue peptides are random coils in aqueous buffer but spontaneously adopt an α-helical conformation in the presence of detergent micelles (sodium dodecyl sulfate, SDS, and perfluorooctanoate, PFO). Furthermore, fluorescence resonance energy transfer experiments, combined with polyacrylamide gel electrophoresis, demonstrate that while γ-TM does not self-associate in SDS, it forms oligomers in PFO, a detergent that tolerates relatively weak associations between membrane proteins. Importantly, oligomerization of γ-TM is abrogated in a peptide that contains either the disease-causing mutation G41R, or the more conservative mutation G41L. On the other hand, a peptide that contains a Gly-to-Arg substitution on a different face of the helix, at position 35, retains its ability to oligomerize. Our results provide evidence for a link between renal hypomagnesaemia and γ subunit oligomerization.     

Conduction pathways in microtubules, biological quantum computation, and consciousness.

Technological computation is entering the quantum realm, focusing attention on biomolecular information processing systems such as proteins, as presaged by the work of Michael Conrad. Protein conformational dynamics and pharmacological evidence suggest that protein conformational states-fundamental information units ('bits') in biological systems-are governed by quantum events, and are thus perhaps akin to quantum bits ('qubits') as utilized in quantum computation. 'Real time' dynamic activities within cells are regulated by the cell cytoskeleton, particularly microtubules (MTs) which are cylindrical lattice polymers of the protein tubulin. Recent evidence shows signaling, communication and conductivity in MTs, and theoretical models have predicted both classical and quantum information processing in MTs. In this paper we show conduction pathways for electron mobility and possible quantum tunneling and superconductivity among aromatic amino acids in tubulins. The pathways within tubulin match helical patterns in the microtubule lattice structure, which lend themselves to topological quantum effects resistant to decoherence. The Penrose-Hameroff 'Orch OR' model of consciousness is reviewed as an example of the possible utility of quantum computation in MTs.     

Increased frequency of scale anomalies and loss of genetic variation in serially bottlenecked populations of the dice snake, Natrix tessellata

Documented demographic bottlenecks resultingfrom introductions of the dice snake to severallakes in Switzerland provide a rare opportunityto study the effect of serial bottlenecks onthe genetic properties of Natrixtessellata populations. We investigated twointroduced populations using informationderived from eight microsatellite markers. Bothintroduced populations had significantlyreduced levels of allelic diversity relative tonon-bottlenecked populations. The severity ofthe bottlenecks was underlined by thesignificant reduction in observed and expectedheterozygosity. The loss of allelic diversityand observed heterozygosity was stronger in theserially bottlenecked population than in thepopulation that was bottlenecked only once.From previous studies, scale anomalies wereknown to be more common in introducedpopulations relative to native populations. Weinvestigated whether the higher occurrence ofscale anomalies in introduced populations isassociated with individual heterozygosity andmean genomic diversity d ². We founda significant relationship between theoccurrence of scale anomalies and individualheterozygosity but no significant relationshipbetween scale anomalies and the microsatellitespecific measurement, d ², was found.Because of their known history, introducedpopulations in Switzerland may serve as a modelto demonstrate the effect of severe populationbottlenecks on genetic variability anddevelopmental stability in N. tessellata.The results therefore help to device strategiesfor the management and protection of endangerednatural N. tessellata populations.     

One hundred years ago: Presents from patient

ObjectiveTo compare rates of upper gastrointestinal haemorrhage among elderly patients given selective cyclo-oxygenase-2 (COX 2) inhibitors and non-selective non-steroidal anti-inflammatory drugs (NSAIDs).DesignObservational cohort study.SettingAdministrative data from Ontario, Canada, used from 17 April 2000 to 31 March 2001 to identify population based, NSAID-naive cohorts of patients.PatientsSubjects aged ⩾66 years who started taking non-selective NSAIDs (n=5391), diclofenac plus misoprostol (n=5087), rofecoxib (n=14 583), or celecoxib (n=18 908) and a randomly selected control cohort not exposed to NSAIDs (n=100 000).ResultsRelative to controls, the multivariate model revealed an increased short term risk of upper gastrointestinal haemorrhage for users of non-selective NSAIDs (adjusted rate ratio 4.0 (95% confidence intervals 2.3 to 6.9)), diclofenac plus misoprostol (3.0 (1.7 to 5.6)), and rofecoxib (1.9 (1.3 to 2.8)) but not celecoxib (1.0 (0.7 to 1.6)). Relative to celecoxib, significantly higher risks of upper gastrointestinal haemorrhage were observed for non-selective NSAIDs (4.4 (2.3 to 8.5)), diclofenac plus misoprostol (3.2 (1.6 to 6.5)), and rofecoxib (1.9 (1.2 to 2.8)). Relative to rofecoxib, non-selective NSAID users were at significantly higher risk of upper gastrointestinal haemorrhage (1.9 (1.0 to 3.5)).ConclusionsThis population based observational study found a lower short term risk of upper gastrointestinal haemorrhage for selective COX-2 inhibitors compared with non-selective NSAIDs.

What is already known on this topic

Long term NSAID use is associated with the development of peptic and duodenal ulcersSelective COX 2 inhibitors are claimed to cause fewer gastrointestinal problems than conventional, non-selective NSAIDsIt is unclear to what degree COX 2 inhibitors increase gastrointestinal risk relative to not using NSAIDs, and the relative gastrointestinal safety of the different COX 2 inhibitors is uncertain

What this study adds

The risk of upper gastrointestinal haemorrhage with the COX 2 inhibitors rofecoxib and celecoxib was significantly lower than with conventional NSAIDs, but the risk with rofecoxib was significantly higher than that with celecoxibThe risk of gastrointestinal haemorrhage with celecoxib was similar to that in controls not using NSAIDs     

Test for positional candidate genes for body composition on pig chromosome 6

One QTL affecting backfat thickness (BF), intramuscular fat content (IMF) and eye muscle area (MA) was previously localized on porcine chromosome 6 in an F₂ cross between Iberian and Landrace pigs. This work was done to study the effect of two positional candidate genes on these traits: H-FABP and LEPR genes. The QTL mapping analysis was repeated with a regression method using genotypes for seven microsatellites and two PCR-RFLPs in the H-FABP and LEPR genes. H-FABP and LEPR genes were located at 85.4 and 107 cM respectively, by linkage analysis. The effects of the candidate gene polymorphisms were analyzed in two ways. When an animal model was fitted, both genes showed significant effects on fatness traits, the H-FABP polymorphism showed significant effects on IMF and MA, and the LEPR polymorphism on BF and IMF. But when the candidate gene effect was included in a QTL regression analysis these associations were not observed, suggesting that they must not be the causal mutations responsible for the effects found. Differences in the results of both analyses showed the inadequacy of the animal model approach for the evaluation of positional candidate genes in populations with linkage disequilibrium, when the probabilities of the parental origin of the QTL alleles are not included in the model.     

A review and appraisal of the DNA damage theory of ageing

Given the central role of DNA in life, and how ageing can be seen as the gradual and irreversible breakdown of living systems, the idea that damage to the DNA is the crucial cause of ageing remains a powerful one. DNA damage and mutations of different types clearly accumulate with age in mammalian tissues. Human progeroid syndromes resulting in what appears to be accelerated ageing have been linked to defects in DNA repair or processing, suggesting that elevated levels of DNA damage can accelerate physiological decline and the development of age-related diseases not limited to cancer. Higher DNA damage may trigger cellular signalling pathways, such as apoptosis, that result in a faster depletion of stem cells, which in turn contributes to accelerated ageing. Genetic manipulations of DNA repair pathways in mice further strengthen this view and also indicate that disruption of specific pathways, such as nucleotide excision repair and non-homologous end joining, is more strongly associated with premature ageing phenotypes. Delaying ageing in mice by decreasing levels of DNA damage, however, has not been achieved yet, perhaps due to the complexity inherent to DNA repair and DNA damage response pathways. Another open question is whether DNA repair optimization is involved in the evolution of species longevity, and we suggest that the way cells from different organisms respond to DNA damage may be crucial in species differences in ageing. Taken together, the data suggest a major role of DNA damage in the modulation of longevity, possibly through effects on cell dysfunction and loss, although understanding how to modify DNA damage repair and response systems to delay ageing remains a crucial challenge.