Lovesick: immunological costs of mating to male sagebrush crickets

A growing body of evidence suggests that resources invested in reproduction often come at the expense of the ability to mount an immune response. During mating, female sagebrush crickets, Cyphoderris strepitans, consume the ends of the male’s hind wings and ingest his haemolymph. Previous research has shown that this behaviour impairs the ability of males to secure additional matings. One hypothesis to account for this effect is that wing wounding triggers an energetically costly immune response, such that nonvirgin males are unable to sustain the costly acoustical signalling needed to attract additional females. To test this hypothesis, we injected virgin males with lipopolysaccharides (LPS) to provoke an immune response, and monitored their mating success in the field. LPS‐injected virgin males took significantly longer to mate than sham‐injected virgin males, and spent significantly less time calling. We also compared virgin, nonvirgin and experimentally wing‐wounded virgin males with respect to: (1) their ability to encapsulate a foreign invader via the accumulation of haemocytes and deposition of melanin and (2) baseline levels of phenoloxidase (PO), a key enzyme in the biochemical cascade leading to the production of melanin. Although encapsulation ability did not differ with reproductive experience, virgin males had significantly higher levels of PO than either nonvirgin or experimentally wing‐wounded virgin males. These results suggest that wing‐wounding alone is sufficient to impair male immunity, and that males trade‐off investment in reproduction and immunity.     

Synthesis of Two Natural Salmon Calcitonins

The structure of calcitonin isolated from salmon¹ (SCT 1) has been recently established² and confirmed by synthesis⁸. It possesses an exceptionally high level of activity, exhibiting about 20–50 times the hypocalcaemic potency of any other calcitonin isolated from mammalian species.     

Haplotype estimation from fuzzy genotypes using penalized likelihood

The Composite Link Model is a generalization of the generalized linear model in which expected values of observed counts are constructed as a sum of generalized linear components. When combined with penalized likelihood, it provides a powerful and elegant way to estimate haplotype probabilities from observed genotypes. Uncertain ("fuzzy") genotypes, like those resulting from AFLP scores, can be handled by adding an extra layer to the model. We describe the model and the estimation algorithm. We apply it to a data set of accurate human single nucleotide polymorphism (SNP) and to a data set of fuzzy tomato AFLP scores.     

Heterologous expression, purification, and biochemistry of the oligomycin sensitivity conferring protein (OSCP) from yeast.

Yeast Saccharomyces cerevisiae oligomycin sensitivity conferring proteins (OSCP) have been expressed in Escherichia coli. Heterologous expression results in production of a protein that is identical to yeast mature OSCP, including the absence of the initiating methionine residue. Yeast OSCP expressed in E. coli has been purified to homogeneity and it is able to reconstitute oligomycin-sensitive ATPase using purified F1- and F1/OSCP-depleted membranes (electron transport particles (ETP). Binding of F1 to ETP is dependent on the addition of OSCP. Binding studies using 35S-OSCP indicated that OSCP binds to ETP with a Kd of 200 nM and a capacity of 420 pmol/mg particle protein, whereas OSCP does not interact with F1 in the absence of ETP. These data indicate that yeast OSCP must first form a specific complex with F0, which then binds F1 forming the functional complex. To identify functional domains in yeast OSCP, two deletion mutants have been made. Antibodies directed to these deletion products do not inhibit OSCP-dependent binding of F1 to ETP. However, antibodies directed against the last one-third of OSCP greatly reduce the oligomycin sensitivity of the reconstituted ATPase. These data suggest that OSCP is involved in a functional role in energy transduction or proton translocation and serves a structural role in the yeast mitochondrial ATP synthase.     

The rhodopsin system of the squid

Squid rhodopsin (λ_max 493 mµ)—like vertebrate rhodopsins—contains a retinene chromophore linked to a protein, opsin. Light transforms rhodopsin to lumi- and metarhodopsin. However, whereas vertebrate metarhodopsin at physiological temperatures decomposes into retinene and opsin, squid metarhodopsin is stable. Light also converts squid metarhodopsin to rhodopsin. Rhodopsin is therefore regenerated from metarhodopsin in the light. Irradiation of rhodopsin or metarhodopsin produces a steady state by promoting the reactions, See PDF for Equation Squid rhodopsin contains neo-b (11-cis) retinene; metarhodopsin all-trans retinene. The interconversion of rhodopsin and metarhodopsin involves only the stereoisomerization of their chromophores. Squid metarhodopsin is a pH indicator, red (λ_max 500 mµ) near neutrality, yellow (λ_max 380 mµ) in alkaline solution. The two forms—acid and alkaline metarhodopsin—are interconverted according to the equation, Alkaline metarhodopsin + H⁺ acid metarhodopsin, with pK 7.7. In both forms, retinene is attached to opsin at the same site as in rhodopsin. However, metarhodopsin decomposes more readily than rhodopsin into retinene and opsin. The opsins apparently fit the shape of the neo-b chromophore. When light isomerizes the chromophore to the all-trans configuration, squid opsin accepts the all-trans chromophore, while vertebrate opsins do not and hence release all-trans retinene. Light triggers vision by affecting directly the shape of the retinene chromophore. This changes its relationship with opsin, so initiating a train of chemical reactions.     

Delay and failure in treatment seeking after first onset of mental disorders in the World Health Organization's World Mental Health Survey Initiative

Data are presented on patterns of failure and delay in making initial treatmentcontact after first onset of a mental disorder in 15 countries in the WorldHealth Organization (WHO)''s World Mental Health (WMH) Surveys. Representativeface-to-face household surveys were conducted among 76,012 respondents aged18 and older in Belgium, Colombia, France, Germany, Israel, Italy, Japan,Lebanon, Mexico, the Netherlands, New Zealand, Nigeria, People''s Republicof China (Beijing and Shanghai), Spain, and the United States. The WHO CompositeInternational Diagnostic Interview (CIDI) was used to assess lifetime DSM-IVanxiety, mood, and substance use disorders. Ages of onset for individual disordersand ages of first treatment contact for each disorder were used to calculatethe extent of failure and delay in initial help seeking. The proportion oflifetime cases making treatment contact in the year of disorder onset rangedfrom 0.8 to 36.4% for anxiety disorders, from 6.0 to 52.1% for mood disorders,and from 0.9 to 18.6% for substance use disorders. By 50 years, the proportionof lifetime cases making treatment contact ranged from 15.2 to 95.0% for anxietydisorders, from 7.9 to 98.6% for mood disorders, and from 19.8 to 86.1% forsubstance use disorders. Median delays among cases eventually making contactranged from 3.0 to 30.0 years for anxiety disorders, from 1.0 to 14.0 yearsfor mood disorders, and from 6.0 to 18.0 years for substance use disorders.Failure and delays in treatment seeking were generally greater in developingcountries, older cohorts, men, and cases with earlier ages of onset. Theseresults show that failure and delays in initial help seeking are pervasiveproblems worldwide. Interventions to ensure prompt initial treatment contactsare needed to reduce the global burdens and hazards of untreated mental disorders.