Physical interpretation of the reference features in textural fractography of fatigue fractures

Reference features of a fatigue fracture surface are the reference texture and reference crack growth rate which are unambiguously mutually related. The reference texture is a subset of the image texture in SEM fractographs. It is expected to be common to all fractures caused by loadings in which significant events occur sufficiently regularly and frequently. The ratio of the reference and the conventional crack growth rate called reference factor is a characteristic of a particular loading. Its value may be related to the sequence of successive sizes of the cyclic plastic zone, while the mechanism of the effect of overloads follows the models of Wheeler and Willenborg. Application to a set of nine test specimens from aluminium alloy loaded by three different loading regimes is shown.

Biological phenotypes underpin the physio-somatic symptoms of somatization, depression, and chronic fatigue syndrome

Objective
Somatization is a symptom cluster characterized by ‘psychosomatic’ symptoms, that is, medically unexplained symptoms, and is a common component of other conditions, including depression and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). This article reviews the data regarding the pathophysiological foundations of ‘psychosomatic’ symptoms and the implications that this has for conceptualization of what may more appropriately be termed physio-somatic symptoms.

Method
This narrative review used papers published in PubMed, Scopus, and Google Scholar electronic databases using the keywords: depression and chronic fatigue, depression and somatization, somatization and chronic fatigue syndrome, each combined with inflammation, inflammatory, tryptophan, and cell-mediated immune (CMI).

Results
The physio-somatic symptoms of depression, ME/CFS, and somatization are associated with specific biomarkers of inflammation and CMI activation, which are correlated with, and causally linked to, changes in the tryptophan catabolite (TRYCAT) pathway. Oxidative and nitrosative stress induces damage that increases neoepitopes and autoimmunity that contribute to the immuno-inflammatory processes. These pathways are all known to cause physio-somatic symptoms, including fatigue, malaise, autonomic symptoms, hyperalgesia, intestinal hypermotility, peripheral neuropathy, etc.

Conclusion
Biological underpinnings, such as immune-inflammatory pathways, may explain, at least in part, the occurrence of physio-somatic symptoms in depression, somatization, or myalgic encephalomyelitis/chronic fatigue syndrome and thus the clinical overlap among these disorders.

Sitting behaviour-based pattern recognition for predicting driver fatigue

The proposed approach based on physiological characteristics of sitting behaviours and sophisticated machine learning techniques would enable an effective and practical solution to driver fatigue prognosis since it is insensitive to the illumination of driving environment, non-obtrusive to driver, without violating driver’s privacy, more acceptable by drivers.

Cognitive function in young people with chronic fatigue syndrome

The study was designed to investigate cognitive function in adolescents and young adults with Chronic Fatigue Syndrome (CFS). CFS patients performed less well on measures of executive function, attention, and memory compared to participants without CFS. Processing speed was similar for both groups and CFS patients achieved higher academic scores.

Development and assessment of an incremental fatigue protocol for contemporary dance

Nine trained contemporary dancers performed a modality-specific, heart-rate-monitored, choreographed fatiguing dance protocol with an assumption of fatigue at volitional exhaustion (RPE 16). Postural stability was assessed as the variability of ground reaction forces and the centre of pressure during the performance of a flat-foot arabesque. Psychological response was assessed using self-reported fatigue, psychological distress (PD), and psychological well-being (PWB) (Subjective Exercise Experience Scale). After reaching RPE 16 in 15.7 ± 2.6 mins, heart rate decreased to the post-warm-up level within 64 ± 9 sec. Variability of ground reaction forces or the centre of pressure was not changed. There were no significant changes in fatigue, psychological distress, or psychological well-being. Within fatigue, there was a significant increase in the item tired (p = 0.04). As supported by the heart rate data and RPE, the protocol achieved an appropriate level of physical demand. No changes in the stability indices were observed, possibly attributed to the rapid recovery in heart rate. The expression of only tiredness suggests the use of a disassociative attentional style by the dancers. The project represents pilot work toward the validation of a monitoring process that supports dancer health and awareness training.

Phase and crystal orientation study of a TRansformation Induced Plasticity steel subjected to cyclic load induced fatigue

An electron backscatter diffraction (EBSD) study of the microstructure of TRIP steel during fatigue failure. Phase and crystal orientation study of a TRIP steel subjected to cyclic load induced fatigue. The relative fractions of austenite, ferrite and martensite are quantified within the strain field of a fatigue crack tip. This data is a subset of data supporting a wider study of the fatigue properties of multiphase steels used in the automotive industry. The different microstructural phases present in these steels can influence the strain life and cyclic stabilized strength of the material due to the way in which these phases accommodate the applied cyclic strain. Fully reversed strain-controlled low-cycle fatigue tests have been used to determine the mechanical fatigue performance of a dual-phase (DP) 590 and transformation induced plasticity (TRIP) 780 steel, with transmission electron microscopy (TEM) and scanning electron microscopy (SEM-EBSD) used to examine the deformed microstructures .

Evidence for the existence of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) with and without abdominal discomfort (irritable bowel) syndrome.

There is evidence that Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is accompanied by gastro-intestinal symptoms; and IgA and IgM responses directed against lipopolysaccharides (LPS) of commensal bacteria, indicating bacterial translocation.

Central pathways causing fatigue in neuro-inflammatory and autoimmune illnesses

The genesis of severe fatigue and disability in people following acute pathogen invasion involves the activation of Toll-like receptors followed by the upregulation of proinflammatory cytokines and the activation of microglia and astrocytes. Many patients suffering from neuroinflammatory and autoimmune diseases, such as multiple sclerosis, Parkinson's disease and systemic lupus erythematosus, also commonly suffer from severe disabling fatigue. Such patients also present with chronic peripheral immune activation and systemic inflammation in the guise of elevated proinflammtory cytokines, oxidative stress and activated Toll-like receptors. This is also true of many patients presenting with severe, apparently idiopathic, fatigue accompanied by profound levels of physical and cognitive disability often afforded the non-specific diagnosis of chronic fatigue syndrome.

The neuro-immune pathophysiology of central and peripheral fatigue in systemic immune-inflammatory and neuro-immune diseases

Many patients with systemic immune-inflammatory and neuro-inflammatory disorders, including depression, rheumatoid arthritis, systemic lupus erythematosus, Sjögren's disease, cancer, cardiovascular disorder, Parkinson's disease, multiple sclerosis, stroke, and chronic fatigue syndrome/myalgic encephalomyelitis, endure pathological levels of fatigue. The aim of this narrative review is to delineate the wide array of pathways that may underpin the incapacitating fatigue occurring in systemic and neuro-inflammatory disorders. A wide array of immune, inflammatory, oxidative and nitrosative stress (O&NS), bioenergetic, and neurophysiological abnormalities are involved in the etiopathology of these disease states and may underpin the incapacitating fatigue that accompanies these disorders. This range of abnormalities comprises: increased levels of pro-inflammatory cytokines, e.g., interleukin-1 (IL-1), IL-6, tumor necrosis factor (TNF) α and interferon (IFN) α; O&NS-induced muscle fatigue; activation of the Toll-Like Receptor Cycle through pathogen-associated (PAMPs) and damage-associated (DAMPs) molecular patterns, including heat shock proteins; altered glutaminergic and dopaminergic neurotransmission; mitochondrial dysfunctions; and O&NS-induced defects in the sodium-potassium pump. Fatigue is also associated with altered activities in specific brain regions and muscle pathology, such as reductions in maximum voluntary muscle force, downregulation of the mitochondrial biogenesis master gene peroxisome proliferator-activated receptor gamma coactivator 1-alpha, a shift to glycolysis and buildup of toxic metabolites within myocytes. As such, both mental and physical fatigue, which frequently accompany immune-inflammatory and neuro-inflammatory disorders, are the consequence of interactions between multiple systemic and central pathways.

The putative role of viruses, bacteria, and chronic fungal biotoxin exposure in the genesis of intractable fatigue accompanied by cognitive and physical disability

Patients who present with severe intractable apparently idiopathic fatigue accompanied by profound physical and or cognitive disability present a significant therapeutic challenge. The effect of psychological counseling is limited, with significant but very slight improvements in psychometric measures of fatigue and disability but no improvement on scientific measures of physical impairment compared to controls. Similarly, exercise regimes either produce significant, but practically unimportant, benefit or provoke symptom exacerbation. Many such patients are afforded the exclusionary, non-specific diagnosis of chronic fatigue syndrome if rudimentary testing fails to discover the cause of their symptoms. More sophisticated investigations often reveal the presence of a range of pathogens capable of establishing life-long infections with sophisticated immune evasion strategies, including Parvoviruses, HHV6, variants of Epstein-Barr, Cytomegalovirus, Mycoplasma, and Borrelia burgdorferi. Other patients have a history of chronic fungal or other biotoxin exposure. Herein, we explain the epigenetic factors that may render such individuals susceptible to the chronic pathology induced by such agents, how such agents induce pathology, and, indeed, how such pathology can persist and even amplify even when infections have cleared or when biotoxin exposure has ceased. The presence of active, reactivated, or even latent Herpes virus could be a potential source of intractable fatigue accompanied by profound physical and or cognitive disability in some patients, and the same may be true of persistent Parvovirus B12 and mycoplasma infection. A history of chronic mold exposure is a feasible explanation for such symptoms, as is the presence of B. burgdorferi. The complex tropism, life cycles, genetic variability, and low titer of many of these pathogens makes their detection in blood a challenge. Examination of lymphoid tissue or CSF in such circumstances may be warranted.

Effect of martensite volume fraction on low cycle fatigue behaviour of dual phase steels: experimental and microstructural investigation

The low cycle fatigue (LCF) behaviour of a dual phase (DP) steel with different martensite volume fractions has been investigated, with particular focus on fatigue life, cyclic hardening/softening behaviour and microstructural evolution. DP steels with martensite volume fractions between 13% and 88% were produced and their monotonic and cyclic deformation behaviours evaluated. The LCF life has been examined in depth and compared with published literature. It has been concluded that, once normalised for plastic strain amplitude, the fatigue life was found to be significantly reduced by an increase in the martensite volume fraction. All alloys were observed to show some initial cyclic hardening followed by cyclic softening. Clear sub-cell formation occurred in ferrite grains irrespective of the martensite volume fraction, and it is suggested that this cell formation and martensite softening are responsible for the cyclic softening behaviour.