The organisation of the stress response, and its relevance to chiropractors: a commentary

The stress response is a natural reaction by the body, against potentially harmful stimuli to enhance the chance for survival. Persistent activation of the stress response can cause changes to homeostatic mechanisms. The study of stress neurophysiology, in the evaluation of the manifestation of disease in the body, suggests that these chronic changes have detrimental effects on sub cortical structures. Furthermore, there is much scientific support for the notion that chronic activation of supraspinal systems will lead to maladaptation of homeostatic mechanisms, causing the impairment of processes within the body, and ultimately leading to visceral disorders. The chiropractic profession for many years has alluded to chronic change of neurophysiological pathways as a potential explanation of visceral disorders, but the profession has typically described these in terms of somatovisceral or viscerosomatic reflex activity. Change in supraspinal neurophysiological efferent activity is increasingly being used to explain "stress" related disease. The chiropractic profession should consider investigating such stress responses by conducting spinal manipulative therapy trials that evaluate supraspinal effects of manipulation. Such research may help elucidate key mechanisms associated with the change of visceral disorders noted by some chiropractors following manipulative therapy

Quantum Locality?

Robert Griffiths has recently addressed, within the framework of a 'consistent quantum theory' that he has developed, the issue of whether, as is often claimed, quantum mechanics entails a need for faster-than-light transfers of information over long distances. He argues that the putative proofs of this property that involve hidden variables include in their premises some essentially classical-physics-type assumptions that are fundamentally incompatible with the precepts of quantum physics. One cannot logically prove properties of a system by establishing, instead, properties of a system modified by adding properties alien to the original system. Hence Griffiths' rejection of hidden-variable-based proofs is logically warranted. Griffiths mentions the existence of a certain alternative proof that does not involve hidden variables, and that uses only macroscopically described observable properties. He notes that he had examined in his book proofs of this general kind, and concluded that they provide no evidence for nonlocal influences. But he did not examine the particular proof that he cites. An examination of that particular proof by the method specified by his 'consistent quantum theory' shows that the cited proof is valid within that restrictive version of quantum theory. An added section responds to Griffiths' reply, which cites general possibilities of ambiguities that make what is to be proved ill-defined, and hence render the pertinent 'consistent framework' ill defined. But the vagaries that he cites do not upset the proof in question, which, both by its physical formulation and by explicit identification, specify the framework to be used. Griffiths confirms the validity of the proof insofar as that framework is used. The section also shows, in response to Griffiths' challenge, why a putative proof of locality that he has described is flawed.Comment: This version adds a response to Griffiths' reply to my original. It notes that Griffiths confirms the validity of my argument if one uses the framework that I use. Griffiths' objection that other frameworks exist is not germaine, because I use the unique one that satisfies the explicitly stated conditions that the choices be macroscopic choices of experiments and outcomes in a specified orde

Fannie Hardy Eckstorm Correspondence

Entries include a typed letter from the Office of the Director of the Field Museum of Natural History in Chicago, a request from the Maine State Librarian for help writing a paper, typed and handwritten correspondence between Eckstorm and the Maine State Library some on personal stationery, a typed description of a folk-song collection on the way to the publisher, a call for traditional versions of songs and their airs, Eckstorm\u27s typed biographical sketches of Smyth and Barry, a newspaper review clipping, and a publisher advertisemen

The stellar populations of spiral disks.II Measuring and modeling the radial distribution of absorption spectral indices

The radial distributions of the Mg2 and Fe5270 Lick spectral indices have been measured to large radial distances on the disks of NGC 4303 and NGC 4535 using an imaging technique based on interference filters. These data, added to those of NGC 4321 previously published in Paper I of this series are used to constraint chemical (multiphase) evolutionary models for these galaxies. Because the integrated light of a stellar disk is a time average over the history of the galaxy weighted by the star formation rate, these constraints complement the information on chemical gradients provided by the study of HII regions which, by themselves, can only provide the alpha-elements abundance accumulate over the life of the galaxy. The agreement between the observations and the model predictions shown here lends confidence to the models which are then used to describe the time evolution of galaxy parameters such as star formation rates, chemical gradients, and gradients in the mean age of the stellar population.Comment: to be published in Astrophysical Journa

Low back pain in junior Australian Rules football: a cross-sectional survey of elite juniors, non-elite juniors and non-football playing controls

<p>Abstract</p> <p>Background</p> <p>Low back pain in junior Australian Rules footballers has not been investigated despite findings that back pain is more prevalent, severe and frequent in senior footballers than non-athletic controls and findings that adolescent back pain is a strong predictor for adult back pain. The aim of this study was to determine the prevalence, intensity, quality and frequency of low back pain in junior Australian Rules footballers and a control group and to compare this data between groups.</p> <p>Methods</p> <p>A cross-sectional survey of male non-elite junior (n = 60) and elite junior players (n = 102) was conducted along with a convenience sample of non-footballers (school children) (n = 100). Subjects completed a self-reported questionnaire on low back pain incorporating the Quadruple Visual Analogue Scale and McGill Pain Questionnaire (short form), along with additional questions adapted from an Australian epidemiological study. Linear Mixed Model (Residual Maximum Likelihood) methods were used to compare differences between groups. Log-linear models were used in the analysis of contingency tables.</p> <p>Results</p> <p>For current, average and best low back pain levels, elite junior players had higher pain levels (p < 0.001), with no difference noted between non-elite juniors and controls for average and best low back pain. For low back pain at worst, there were significant differences in the mean pain scores. The difference between elite juniors and non-elite juniors (p = 0.040) and between elite juniors and controls (p < 0.001) was significant, but not between non-elite juniors and controls. The chance of suffering low back pain increases from 45% for controls, through 55% for non-elite juniors to 66.7% for elite juniors. The chance that a pain sufferer experiences chronic pain is 16% for controls and 41% for non-elite junior and elite junior players. Elite junior players experienced low back pain more frequently (p = 0.002), with no difference in frequency noted between non-elite juniors and controls. Over 25% of elite junior and non-elite junior players reported that back pain impacted their performance some of the time or greater.</p> <p>Conclusions</p> <p>This study demonstrated that when compared with non-elite junior players and non-footballers of a similar age, elite junior players experience back pain more severely and frequently and have higher prevalence and chronicity rates.</p

Integrating protein networks and machine learning for disease stratification in the Hereditary Spastic Paraplegias.

The Hereditary Spastic Paraplegias are a group of neurodegenerative diseases characterized by spasticity and weakness in the lower body. Owing to the combination of genetic diversity and variable clinical presentation, the Hereditary Spastic Paraplegias are a strong candidate for protein-protein interaction network analysis as a tool to understand disease mechanism(s) and to aid functional stratification of phenotypes. In this study, experimentally validated human data were used to create a protein-protein interaction network based on the causative genes. Network evaluation as a combination of topological analysis and functional annotation led to the identification of core proteins in putative shared biological processes, such as intracellular transport and vesicle trafficking. The application of machine learning techniques suggested a functional dichotomy linked with distinct sets of clinical presentations, indicating that there is scope to further classify conditions currently described under the same umbrella-term of Hereditary Spastic Paraplegias based on specific molecular mechanisms of disease

Multimodal perioperative pain protocol for Gynecologic Oncology laparotomy reduces length of hospital stay

Our primary objective was to evaluate the impact of a multimodal perioperative pain regimen on length of hospital stay for patients undergoing laparotomy with a gynecologic oncologist

Gene co-expression networks shed light into diseases of brain iron accumulation

Aberrant brain iron deposition is observed in both common and rare neurodegenerative disorders, including those categorized as Neurodegeneration with Brain Iron Accumulation (NBIA), which are characterized by focal iron accumulation in the basal ganglia. Two NBIA genes are directly involved in iron metabolism, but whether other NBIA-related genes also regulate iron homeostasis in the human brain, and whether aberrant iron deposition contributes to neurodegenerative processes remains largely unknown. This study aims to expand our understanding of these iron overload diseases and identify relationships between known NBIA genes and their main interacting partners by using a systems biology approach. We used whole-transcriptome gene expression data from human brain samples originating from 101 neuropathologically normal individuals (10 brain regions) to generate weighted gene co-expression networks and cluster the 10 known NBIA genes in an unsupervised manner. We investigated NBIA-enriched networks for relevant cell types and pathways, and whether they are disrupted by iron loading in NBIA diseased tissue and in an in vivo mouse model. We identified two basal ganglia gene co-expression modules significantly enriched for NBIA genes, which resemble neuronal and oligodendrocytic signatures. These NBIA gene networks are enriched for iron-related genes, and implicate synapse and lipid metabolism related pathways. Our data also indicates that these networks are disrupted by excessive brain iron loading. We identified multiple cell types in the origin of NBIA disorders. We also found unforeseen links between NBIA networks and iron-related processes, and demonstrate convergent pathways connecting NBIAs and phenotypically overlapping diseases. Our results are of further relevance for these diseases by providing candidates for new causative genes and possible points for therapeutic intervention