Shooting methods for a PT-symmetric periodic eigenvalue problem

We present a rigorous analysis of the performance of some one-step discretization schemes for a class of PT-symmetric singular boundary eigenvalue problem which encompasses a number of different problems whose investigation has been inspired by the 2003 article of Benilov et al. (J Fluid Mech 497:201-224, 2003). These discretization schemes are analyzed as initial value problems rather than as discrete boundary problems, since this is the setting which ties in most naturally with the formulation of the problem which one is forced to adopt due to the presence of an interior singularity. We also devise and analyze a variable step scheme for dealing with the singular points. Numerical results show better agreement between our results and those obtained from small-ε asymptotics than has been shown in results presented hitherto

The adipokines in cancer cachexia

Cachexia is a devastating pathology induced by several kinds of diseases, including cancer. The hallmark of cancer cachexia is an extended weight loss mainly due to skeletal muscle wasting and fat storage depletion from adipose tissue. The latter exerts key functions for the health of the whole organism, also through the secretion of several adipokines. These hormones induce a plethora of effects in target tissues, ranging from metabolic to differentiating ones. Conversely, the decrease of the circulating level of several adipokines positively correlates with insulin resistance, metabolic syndrome, diabetes, and cardiovascular disease. A lot of findings suggest that cancer cachexia is associated with changed secretion of adipokines by adipose tissue. In agreement, cachectic patients show often altered circulating levels of adipokines. This review reported the findings of adipokines (leptin, adiponectin, resistin, apelin, and visfatin) in cancer cachexia, highlighting that to study in-depth the involvement of these hormones in this pathology could lead to the development of new therapeutic strategies

Transcranial sonography in the diagnosis, follow-up and treatment of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

We used a modified transcranial sonography technique to study the cortex of the temporal lobe, a brain region involved in the processing of functions that are often compromised in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) patients. We studied the meninges, the subarachnoidal space and the cortex. The spatial resolution and the ability to visualize structures of 200-300 µm size, led us to hypothesize that the linear structures parallel to the subarachnoidal space could be referred to the neuronal layers of the cortex. In real-time mode, we could observe pulsation of the meninges and the cortex synchronous with the heart beat and independent of blood flow. This pulsation was more evident at the level of the meninges, but it was also appreciable at the level of the layers of the cortex and it was not accompanied by any type of flow. In addition to these findings, we observed that the subject undergoing the procedure experienced a series of changes that might prove potentially useful in the treatment of ME/CFS. In particular, we observed a decrease of tachycardia accompanied by an increase in systolic blood pressure and by a significant increase in muscle strength measured by the degree of muscle fibre shortening at the level of the biceps brachii. These findings, together with the low cost and simplicity of the procedure, suggest that modified transcranial sonography has a significant potential in the study and treatment of ME/CFS

An integrated analysis of the effects of Esculentin 1-21 on Saccharomyces cerevisiae.

The antimicrobial peptide esculentin 1–21 (Esc 1–21) is a shorter synthetic version of the 46-residue peptide occurring in the Rana esculenta skin secretion. Here we propose an integrated proteomic and transcriptomic approach to interpret the biological effects of this peptide on Saccharomyces cerevisiae. We further investigated the response to this peptide by correlating the results of the transcriptome and proteome analysis with phenotypic effects. The results show that S. cerevisiae adapts to Esc 1–21 using the High Osmolarity Glycerol (HOG) pathway involved in osmotic tolerance and cell wall maintenance. Comparative proteomics reveals that Esc 1–21 causes downregulation of enzymes of the lower glycolytic pathway and in genes involved in spindle body formation and remodelling of cell-wall synthesis. Moreover the peptide induces downexpression of protein actin within 45 min and cells pre-treated with peptide show less sensitivity to osmotic stress and increased sensitivity to heat shock stress. The results obtained with the two different methodologies are in agreement at the cellular process levels. A combined approach may help elucidate the main aspects related to the effects of this peptide on the eukaryotic cell. The employment of different technologies may reveal the potential and limitations of each adapted approach in a prospective application for drug screening

Could cadmium be responsible for some of the neurological signs and symptoms of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

According to the World Health Organization, Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a neurological disease characterized by widespread inflammation and multi-systemic neuropathology. Aetiology and pathogenesis are unknown, and several agents have been proposed as causative agents or as factors perpetuating the syndrome. Exposure to heavy metals, with particular reference to mercury and gold in dental amalgams, has been considered among the triggers of ME/CFS. Here we hypothesize that cadmium, a widespread occupational and environmental heavy metal pollutant, might be associated with some of the neurological findings described in ME/CFS. In fact, ME/CFS patients show a decrease of the volume of the gray matter in turn associated with objective reduction of physical activity. Cadmium induces neuronal death in cortical neurons through a combined mechanism of apoptosis and necrosis and it could then be hypothesized that cadmium-induced neuronal cell death is responsible for some of the effects of cadmium on the central nervous system, i.e. a decrease in attention level and memory in exposed humans as well as to a diminished ability for training and learning in rats, that are symptoms typical of ME/CFS. This hypothesis can be tested by measuring cadmium exposure in a cohort of ME/CFS patients compared with matched healthy controls, and by measuring gray matter volume in un-exposed healthy controls, exposed non-ME/CFS subjects, un-exposed ME/CFS patients and exposed ME/CFS patients. In addition, we hypothesize that cadmium exposure could be associated with reduced cerebral blood flow in ME/CFS patients because of the disruptive effects of cadmium on angiogenesis. In fact, cadmium inhibits angiogenesis and low global cerebral flow is associated with abnormal brain neuroimaging results and brain dysfunction in the form of reduced cognitive testing scores in ME/CFS patients. This hypothesis can be tested by measuring cerebral cortex blood flow in un-exposed healthy controls, exposed non-ME/CFS subjects, un-exposed ME/CFS patients and exposed ME/CFS patients. If our hypothesis is demonstrated correct, the consequences could affect prevention, early diagnosis, and treatment of ME/CFS. Implications in early diagnosis could entail the evaluation of symptoms typical of ME/CFS in cadmium-exposed subjects as well as the search for signs of exposure to cadmium in subjects diagnosed with ME/CFS. Nutritional supplementation of magnesium and zinc could then be considered, since these elements have been proposed in the prophylaxis and therapy of cadmium exposure, and magnesium was demonstrated effective on ME/CFS patients' symptom profiles