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Degeneracy is a poorly understood process, essential to natural selection. In the 18th and 19th centuries, the concept of degeneracy was commandeered by the colonial imagination. A rigid understanding of species, race, and culture grew to dominate the normative thinking that persisted well into the burgeoning new industrial age. A 20th-century reconfiguration of the concept by George Gamow highlighted a form of intraorganismic variation that is still underexplored. Degeneracy exists in a population of variants where structurally different components perform a similar, but not necessarily identical, function with respect to context. The presence of degeneracy increases a system’s complexity and robustness against perturbations. The loss of a genetic component in biological systems, for example, can be compensated by redundant elements (the presence of isomorphic and isofunctional components), or by degenerate elements (heteromorphic variants that are isofunctional). A historical survey of the use of the term “degeneracy” reveals how and why the processes it once designated, and the mechanisms it now represents, have largely escaped the purview of contemporary science. Despite confusion and general oversight, degeneracy has been characterized by select researchers at the molecular, genetic, and neuronal levels. The concept is a potent analytical tool to understand selection, variation, and transmission.

The sexually dimorphic vasopressin system of the bed nucleus of the stria terminalis (BNST) is the most sensitive neurotransmitter system regulated by sex steroids in rats and mice. In addition to vasopressin, the BNST neurons also express a second neuropeptide, galanin, whose expression also appears to be regulated by testosterone in laboratory rodents. Seasonal fluctuations of sex steroids in photoperiodic rodents feed back on the brain to regulate the expression of sex steroid sensitive genes. The seasonal rhythm of circulating sex steroids is generated by photoperiod-controlled melatonin secretion, resulting in a seasonal stimulation and involution of the gonads. We have studied the seasonal expression of vasopressin and galanin in BNST neurons and their target areas in the Djungarian hamster (Phodopus sungorus). Furthermore, we analyzed the effect of testosterone on vasopressin and galanin by testosterone supplementation in animals where reproduction was inhibited by exposure to a short photoperiod. Exposure to short photoperiod induced a major reduction in the expression of vasopressin in BNST neurons, as well as in their target areas, the lateral septum (LS) and the lateral habenula (LHb). Galanin expression in the BNST and its target areas was also strongly reduced, although this reduction did not result in an almost complete disappearance of the neuropeptide as observed for vasopressin. Testosterone was able to reverse this reduction for both vasopressin and galanin. However, while the mRNA expression in BNST neurons recovered within 2-4 days, recovery of the neuropeptide immunoreactivity in the target areas, LS and LHb, required more than 3 weeks. The photoperiod-driven testosterone rhythm thus appears to be a major regulator of extra-hypothalamic vasopressin and galanin in the Djungarian hamster. The long delay between mRNA recovery in the cell body and the neuropeptide recovery in the target areas may be due to progressive filling up of the axon terminals. Alternatively, this delay might be indicative of a seasonal structural plasticity.

This chapter addresses the representational politics of endemicity, arguing provocatively that viruses don’t kill people—people kill people. In pursuit of this claim, the authors develop a framework derived from historical studies of public health and from contemporary research in Structural One Health to argue that endemicity is not a natural phenomenon but is rather produced by social and economic policies. The authors argue that causal relations of endemic disease must be restructured in the popular imaginary. This chapter uses epidemics with isolated examples of “endemic” instances (tuberculosis in particular) to consider hierarchies and levels of cause, how these relate to global political economy, and with what implications for preventive and responsive action.

Albert et al. [1] advocate for a multipronged approach in rolling out new diagnostic technology for tuberculosis (TB), stating “diagnostic tests alone, if not implemented with a comprehensive package of accompanying tools and within the context of a strengthened health system, may fail to demonstrate the expected benefit”. This is a lesson learned from those who have walked this path before us; one should not be too complacent to ignore basic strategies in the face of escalating technological advances in our field., Without societal, lifestyle and dietary innovations, new technologies will be ineffectual in stopping tuberculosis http://ow.ly/IgY3303bgdU

Sleep paralysis: night-mares, nocebos, and the mind-body connection, by Shelley R. Adler, New Jersey, Rutgers University Press, 2011, 168 pp., ISBN 978-0-8135-4886-9 When considering the same psych...

If James has a latent tuberculosis infection (LTBI), he is at risk of developing active tuberculosis disease but he is not yet sick. LTBI is a liminal space between health and illness. Diagnosed with LTBI, James could be conceptualised as having a liminal body. Treatments for LTBI are available, but why would a person seek treatment for a disease he does not yet have? One thing is definite: James needs to be educated about the symptoms and severity of active tuberculosis disease.

Researchers in the field of epigenomics are developing more nuanced understandings of biological complexity, and exploring the multiple pathways that lead to phenotypic expression. The concept of degeneracycreferring to the multiple pathways that a system recruits to achieve functional plasticitycis an important conceptual accompaniment to the growing body of knowledge in epigenomics. Distinct from degradation, redundancy and dilapidation; degeneracy refers to the plasticity of traits whose function overlaps in some environments, but diverges in others. While a redundant system is composed of repeated identical elements performing the same function, a degenerate system is composed of different elements performing similar or overlapping functions. Here, we describe the degenerate structure of gene regulatory systems from the basic genetic code to flexible epigenomic modifications, and discuss how these structural features have contributed to organism complexity, robustness, plasticity and evolvability.

Mikanecic acid derivatives can be prepared in high yield from α-hydroxyalkyl acrylates via an allylic carbamate intermediate.

Reaction of N,N-diethyl cinnamyl carbamate with TBDMSC1 yields the mono-silylated carbamate which, on treatment with butyllithium, reacts with various electrophiles to give the corresponding disubstituted carbamates.

N,N-Diethylbenzyl and cinnamyl carbamates have been found to react with silyl chlorides to give, in some cases, the bis-silylated product, and not the mono-silylated product as previously observed.

Why animal communication displays are so complex and how they have evolved are active foci of research with a long and rich history. Progress towards an evolutionary analysis of signal complexity, however, has been constrained by a lack of hypotheses to explain similarities and/or differences in signalling systems across taxa. To address this, we advocate incorporating a systems approach into studies of animal communication—an approach that includes comprehensive experimental designs and data collection in combination with the implementation of systems concepts and tools. A systems approach evaluates overall display architecture, including how components interact to alter function, and how function varies in different states of the system. We provide a brief overview of the current state of the field, including a focus on select studies that highlight the dynamic nature of animal signalling. We then introduce core concepts from systems biology (redundancy, degeneracy, pluripotentiality, and modularity) and discuss their relationships with system properties (e.g. robustness, flexibility, evolvability). We translate systems concepts into an animal communication framework and accentuate their utility through a case study. Finally, we demonstrate how consideration of the system-level organization of animal communication poses new practical research questions that will aid our understanding of how and why animal displays are so complex.

A new, high yielding route to substituted glutaric acid derivatives via an ester enolate Claisen rearrangement of allylic malonates is described.

Evidence from studies of nuclear and mitochondrial DNA extracted from Neanderthal fossils and humans points to fascinating hypotheses concerning the types of interbreeding that occurred between these two species. Humans and Neanderthals share a small percentage of nuclear DNA. However, humans and Neanderthals do not possess the same mito­chondrial DNA. In mammals, mitochondrial DNA is exclusively maternally inherited. Taking into account an understanding of interspecific hybridity, the available data leads to the hypothesis that only male Neanderthals were able to mate with female humans. If Haldan's Law applied to the progeny of Neanderthals and humans, then female hybrids would survive, but male hybrids would be absent, rare, or sterile. Interbreeding between male Neanderthals and female humans, as the only possible scenario, accounts for the presence of Neanderthal nuclear DNA, the scarcity of Neanderthal Y-linked genes, and the lack of mitochondrial DNA in modern human populations.

A new, high yielding route to substituted glutaric acid derivatives via an ester enolate Claisen rearrangement of allylic malonates is described.

Reaction of N,N-diethyl cinnamyl carbamate with TBDMSC1 yields the mono-silylated carbamate which, on treatment with butyllithium, reacts with various electrophiles to give the corresponding disubstituted carbamates.