Molecular Phylogenetic Relatedness of Frenkelia spp. (Protozoa,Apicomplexa) to Sarcocystis falcatula Stiles 1893: Is the Genus Sarcocystis Paraphyletic?

ABSTRACT The coccidians Frenkelia microti and F. glareoli (Apicomplexa: Sarcocystidae) form tissue cysts in the brain of small rodents (intermediate hosts) while oocysts are formed in the intestine of final hosts, buzzards of the genus Buteo. The inclusion of the small subunit ribosomal RNA gene sequences (SSU rRNA) of both Frenkelia species into the SSU rRNA trees of other, tissue cyst-forming coccidia strongly supports paraphyly of the genus Sarcocystis. Frenkelia spp. exhibit close relatedness to Sarcocystis falcatula Stiles 1893, a bird-opossum parasite, recognized under its junior synonym S. neurona Dubey et al. 1991, as the causative agent of equine protozoan myeloencephalitis on the American continent. As the definition of the genus Frenkelia is based on a plesiomorphic character (affinity to the neural tissue) of supposedly low phylogenetic value, the synonymization of the genus Frenkelia with Sarcocystis is proposed. This renders the genus Sarcocystis monophyletic.     

Macrophage activation and HIV infection: can the Trojan horse turn into a fortress?

Macrophages are infected early during HIV infection and are thought to play the role of a Trojan horse by spreading infection in tissues. Most recent studies point out to a more complex role for macrophages in HIV infection: macrophages could contribute to both host defense and viral persistence and pathogenesis. Infected macrophages are a reservoir for HIV and modulate apoptosis of T cells present in their vicinity. Also, a functional impairment of HIV-infected macrophages may play a role in AIDS pathogenesis. Nevertheless, both activation and differentiation of monocyte/macrophages can interfere with susceptibility of these cells to infection. Therefore, a wide variety of stimuli result in HIV suppression through macrophage activation. At present times, a dynamic view on the role of macrophages in HIV infection arises which indicates that macrophages are a target for the virus and at the same time regulate its replication. Therefore, macrophages are at the cross-road between protection and pathogenesis in HIV infection due to their involvement both as a viral target and a key modulator of non-specific and specific immune responses. Future studies will help unravel the cellular and molecular mechanisms that underlie HIV-macrophage interactions and might result in new vaccine and/or therapeutic strategies.     

Are Treatments More Effective than Placebos? A Systematic Review and Meta-Analysis

BackgroundPlacebos are widely used in clinical practice in spite of ethical restrictions. Whether such use is justified depends in part on the relative benefit of placebos compared to ‘active’ treatments. A direct test for differences between placebo and ‘active’ treatment effects has not been conducted.ObjectivesWe aimed to test for differences between treatment and placebo effects within similar trial populations.ResultsIn trials with continuous outcomes (n = 115) we found no difference between treatment and placebo effects (MD = −0.29, 95% CI −0.62 to 0.05, P = 0.10). In trials with binary outcomes (n = 37) treatments were significantly more effective than placebos (RRR = 0.72, 95%CI = 0.61 to 0.86, P = 0.0003). Treatment and placebo effects were not different in 22 out of 28 predefined subgroup analyses. Of the six subgroups with differences treatments were more effective than placebos in five. However when all criteria for reducing bias were ruled out (continuous outcomes) placebos were more effective than treatments (MD = 1.59, 95% CI = 0.40 to 2.77, P = 0.009).

Conclusions and Implications

Placebos and treatments often have similar effect sizes. Placebos with comparatively powerful effects can benefit patients either alone or as part of a therapeutic regime, and trials involving such placebos must be adequately blinded.     

Isolation and characterization of A new β-melanotropin from horse pituitary glands

A new β-melanotropin was isolated from horse pituitaries and its primary structure has been determined. The amino acid sequence of the new peptide differed from that of β-melanotropin in the deletion of the NH₂-terminal aspartic acid. Thus, it is designated as [Des-Asp¹]-β-melanotropin. It possessed higher lipolytic activity when compared with β-melanotropin.     

Low temperature thresholds: are chill coma and CT(min) synonymous?

The effects of sub-lethal low temperatures on insect physiology and behaviour are important determinants of insect activity including foraging, mating, and predation avoidance. A substantial body of research seeks to relate the temperatures at which these activities are compromised to both, climatic conditions at species range limits and underlying physiological processes. The interpretation of this research is complicated by confusion in the names and definition of the responses measured and their associated temperature thresholds. The development of the nomenclature and explanations of the underlying physiological causes are reviewed in order to elucidate the correct sequence of responses/thresholds and associated terminologies. The results of this analysis indicate that: (1) chill coma is a clearly defined, reversible physiological state characterised by the absence of electrophysiological activity. (2) The onset of chill coma begins when low temperatures begin to impair insect behaviour and physiology, and is punctuated by a series of behavioural and/or physiological thresholds or responses. These include the temperatures at which (i) spontaneous movements cease, (ii) coordination is lost to the degree that locomotion becomes impossible, and (iii) chill coma is entered. (3) Confusion has arisen because (a) the term ‘onset of chill coma’ has been used to describe all three of these responses/thresholds and (b) the term CT_min has entered the insect literature from the vertebrate literature. These issues are discussed and a potential solution is proposed to provide clarity and consistency in the future literature.     

Are aposematic signals honest? A review

We explore the relevance of honest signalling theory to the evolution of aposematism. We begin with a general consideration of models of signal stability, with a focus on the Zahavian costly signalling framework. Next, we review early models of signalling in the context of aposematism (some that are consistent and some inconsistent with costly honest signalling). We focus on controversies surrounding the idea that aposematic signals are handicaps in a Zahavian framework. Then, we discuss how the alignment of interests between signaller and predator influences the evolution of aposematism, highlight the distinction between qualitative and quantitative honesty and review theory and research relevant to these categories. We also review recent theoretical treatments of the evolution of aposematism that have focused on honest signalling as well as empirical research on a variety of organisms, including invertebrates and frogs. Finally, we discuss future directions for empirical and theoretical research in this area.     

Climate change and coral reefs: Trojan horse or false prophecy?

Maynard et al. (Coral Reefs 27:745–749, 2008a) claim that much of the concern about the impacts of climate change on coral reefs has been “based on essentially untested assumptions regarding reefs and their capacity to cope with future climate change”. If correct, this claim has important implications for whether or not climate change represents the largest long-term threat to the sustainability of coral reefs, especially given their ad hominem argument that many coral reef scientists are guilty of “popularising worst-case scenarios” at the expense of truth. This article looks critically at the claims made by Maynard et al. (Coral Reefs 27:745–749, 2008a) and comes to a very different conclusion, with the thrust and veracity of their argument being called into question. Contrary to the fears of Grigg (Coral Reefs 11:183–186, 1992), who originally made reference to the Cassandra syndrome due to his concern about the sensationalisation of science, the proposition that coral reefs face enormous challenges from climate change and ocean acidification has and is being established through “careful experimentation, long-term monitoring and objective interpretation”. While this is reassuring, coral reef ecosystems continue to face major challenges from ocean warming and acidification. Given this, it is an imperative that scientists continue to maintain the rigour of their research and to communicate their conclusions as widely and clearly as possible. Given the shortage of time and the magnitude of the problem, there is little time to spare.