Skunk River Review Fall 1997, Vol 9

https://openspace.dmacc.edu/skunkriver/1018/thumbnail.jp

Deception studies manipulating centrally acting performance modifiers: a review.

Athletes anticipatorily set and continuously adjust pacing strategies before and during events to produce optimal performance. Selfregulation ensures maximal effort is exerted in correspondence with the end point of exercise, while preventing physiological changes that are detrimental and disruptive to homeostatic control. The integration of feedforward and feedback information, together with the proposed brain_s performance modifiers is said to be fundamental to this anticipatory and continuous regulation of exercise. The manipulation of central, regulatory internal and external stimuli has been a key focus within deception research, attempting to influence the self-regulation of exercise and induce improvements in performance. Methods of manipulating performance modifiers such as unknown task end point, deceived duration or intensity feedback, self-belief, or previous experience create a challenge within research, as although they contextualize theoretical propositions, there are few ecological and practical approaches which integrate theory with practice. In addition, the different methods and measures demonstrated in manipulation studies have produced inconsistent results. This review examines and critically evaluates the current methods of how specific centrally controlled performance modifiers have been manipulated, within previous deception studies. From the 31 studies reviewed, 10 reported positive effects on performance, encouraging future investigations to explore the mechanisms responsible for influencing pacing and consequently how deceptive approaches can further facilitate performance. The review acts to discuss the use of expectation manipulation not only to examine which methods of deception are successful in facilitating performance but also to understand further the key components used in the regulation of exercise and performance

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead

Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)

In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. For example, a key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process versus those that measure fl ux through the autophagy pathway (i.e., the complete process including the amount and rate of cargo sequestered and degraded). In particular, a block in macroautophagy that results in autophagosome accumulation must be differentiated from stimuli that increase autophagic activity, defi ned as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (inmost higher eukaryotes and some protists such as Dictyostelium ) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the fi eld understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. It is worth emphasizing here that lysosomal digestion is a stage of autophagy and evaluating its competence is a crucial part of the evaluation of autophagic flux, or complete autophagy. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. Along these lines, because of the potential for pleiotropic effects due to blocking autophagy through genetic manipulation it is imperative to delete or knock down more than one autophagy-related gene. In addition, some individual Atg proteins, or groups of proteins, are involved in other cellular pathways so not all Atg proteins can be used as a specific marker for an autophagic process. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field

Spatio-temporal Analysis of Acute Admissions for Ischemic Heart Disease in NSW, Australia

The recently funded Spatial Environment Epidemiology in New south Wales (SEE NSW) project aims to use routinely collected data in NSW Australia to investigate risk factors for various chronic diseases. In this paper, we present a case study focused on the relationship between social disadvantage and ischemic heart disease to highlight some of the methodological challenges that are likely to arise