New insights about the putative role of myokines in the context of cardiac rehabilitation and secondary cardiovascular prevention.

Exercise training prevents the onset and the development of many chronic diseases, acting as an effective tool both for primary and for secondary prevention. Various mechanisms that may be the effectors of these beneficial effects have been proposed during the past decades: some of these are well recognized, others less. Muscular myokines, released during and after muscular contraction, have been proposed as key mediators of the systemic effects of the exercise. Nevertheless the availability of an impressive amount of evidence regarding the systemic effects of muscle-derived factors, few studies have examined key issues: (I) if skeletal muscle cells themselves are the main source of cytokine during exercise; (II) if the release of myokines into the systemic circulation reach an adequate concentration to provide significant effects in tissues far from skeletal muscle; (III) what may be the role carried out by muscular cytokine regarding the well-known benefits induced by regular exercise, first of all the anti-inflammatory effect of exercise. Furthermore, a greater part of our knowledge regarding myokines derives from the muscle of healthy subjects. This knowledge may not necessarily be transferred per se to subjects with chronic diseases implicating a direct or indirect muscular dysfunction and/or a chronic state of inflammation with persistent immune-inflammatory activation (and therefore increased circulating levels of some cytokines): cachexia, sarcopenia due to multiple factors, disability caused by neurological damage, chronic congestive heart failure (CHF) or coronary artery disease (CAD). A key point of future studies is to ascertain how is modified the muscular release of myokines in different categories of unhealthy subjects, both at baseline and after rehabilitation. The purpose of this review is to discuss the main findings on the role of myokines as putative mediators of the therapeutic benefits obtained through regular exercise in the context of secondary cardiovascular prevention

Role of regular physical activity in neuroprotection against acute ischemia

One of the major obstacles that prevents an effective therapeutic intervention against ischemic stroke is the lack of neuroprotective agents able to reduce neuronal damage; this results in frequent evolution towards a long-term disability with limited alternatives available to aid in recovery. Nevertheless, various treatment options have shown clinical efficacy. Neurotrophins such as brain-derived neurotrophic factor (BDNF), widely produced throughout the brain, but also in distant tissues such as the muscle, have demonstrated regenerative properties with the potential to restore damaged neural tissue. Neurotrophins play a significant role in both protection and recovery of function following neurological diseases such as ischemic stroke or traumatic brain injury. Unfortunately, the efficacy of exogenous administration of these neurotrophins is limited by rapid degradation with subsequent poor half-life and a lack of blood–brain-barrier permeability. Regular exercise seems to be a therapeutic approach able to induce the activation of several pathways related to the neurotrophins release. Exercise, furthermore, reduces the infarct volume in the ischemic brain and ameliorates motor function in animal models increasing astrocyte proliferation, inducing angiogenesis and reducing neuronal apoptosis and oxidative stress. One of the most critical issues is to identify the relationship between neurotrophins and myokines, newly discovered skeletal muscle-derived factors released during and after exercise able to exert several biological functions. Various myokines (e.g., Insulin-Like Growth Factor 1, Irisin) have recently shown their ability to protects against neuronal injury in cerebral ischemia models, suggesting that these substances may influence the degree of neuronal damage in part via inhibiting inflammatory signaling pathways. The aim of this narrative review is to examine the main experimental data available to date on the neuroprotective and anti-ischemic role of regular exercise, analyzing also the possible role played by neurotrophins and myokines

New Insights in Prevention and Treatment of Cardiovascular Disease

Cardiovascular (CV) disease (CVD) is still a major cause of morbidity and mortality in many countries in Europe although considerable efforts have been made in recent decades to address this disease in an even more “comprehensive” approac

Hieracium hypochoeroides subsp. montis-scuderii (Asteraceae), a new endemic subspecies from Sicily (Italy)

Hieracium hypochoeroides subsp. montis-scuderii, a new subspecies endemic to Sicily, is described and illustrated. It is only known from the carbonate cliffs of Monte Scuderi (Peloritani Mountains, NE-Sicily). Informations on its ecology and taxonomic relationships are provided

Effects of physical exercise on inflammatory markers of atherosclerosis.

It is well established that physically fit individuals have a reduced risk of developing CVD (cardiovascular disease) and other age-related chronic disorders. Regular exercise is an established therapeutic intervention with an enormous range of benefits. Chronic low-grade systemic inflammation may be involved in atherosclerosis, diabetes and in pathogenesis of several chronic pathological conditions; recent findings confirm that physical activity induces an increase in the systemic levels of a number of cytokines and chemokines with anti-inflammatory properties. The possibility that regular physical exercise exerts anti-inflammation activity, being the interaction between contracting muscle and the other tissues and the circulating cells mediated through signals transmitted by "myokines" produced with muscle contractions. To date the list of myokines includes IL-6, IL-8, and IL-15. During muscle contractions are also released IL-1 receptor antagonis and sTNF-R, molecules that contribute to provide anti-inflammatory actions. Nevertheless discrepancies, analysis of available researches seem to confirm the efficacy of regular physical training as a nonpharmacological therapy having target chronic low-grade inflammation. Given this, physical exercise could be considerate a useful weapon against local vascular and systemic inflammation in atherosclerosis. Several mechanisms explain the positive effect of chronic exercise, nevertheless, these mechanisms do not fully enlighten all pathways by which exercise can decrease inflammation and endothelial dysfunction, and hence modulate the progression of the underlying disease progres

Immuno-inflammatory activation in acute cardio-embolic strokes in comparison with other subtypes of ischaemic stroke

Few studies have examined the relationship between inflammatory biomarker blood levels, cardioembolic stroke subtype and neurological deficit. So the aim of our study is to evaluate plasma levels of immuno-inflammatory variables in patients with cardio-embolic acute ischaemic stroke compared to other diagnostic subtypes and to evaluate the relationship between immuno-inflammatory variables, acute neurological deficit and brain infarct volume. One hundred twenty patients with acute ischaemic stroke and 123 controls without a diagnosis of acute ischaemic stroke were evaluated. The type of acute ischaemic stroke was classified according to the TOAST classification. We evaluated plasma levels of IL-1beta, TNF-alpha, IL-6 and IL-10, E-selectin, P-selectin, sICAM-1,sVCAM-1, vWF, TPA and PAI-1. Patients with ischaemic stroke classified as cardio-embolic (CEI) showed, compared to other subtypes, significantly higher median plasma levels of TNF-alpha , IL-6 and IL-1beta. Furthermore stroke patients classified as lacunar showed, compared to other subtypes, significantly lower median plasma levels of TNF-alpha, IL-6 and IL-1beta. Multiple linear regression showed a significant association between the Scandinavian Stroke Scale (SSS) score at admission and diagnostic subtype, infarct volume of cardio-embolic strokes and some inflammatory variables. Our findings confirm that cardio-embolic strokes have a worse clinical presentation and produce larger and more disabling strokes than other ischaemic stroke subtypes reporting a possible explanation of higher immuno-inflammatory activation of the acute phase.Few studies have examined the relationship between inflammatory biomarker blood levels, cardioembolic stroke subtype and neurological deficit. So the aim of our study is to evaluate plasma levels of immuno-inflammatory variables in patients with cardio-embolic acute ischaemic stroke compared to other diagnostic subtypes and to evaluate the relationship between immuno-inflammatory variables, acute neurological deficit and brain infarct volume. One hundred twenty patients with acute ischaemic stroke and 123 controls without a diagnosis of acute ischaemic stroke were evaluated. The type of acute ischaemic stroke was classified according to the TOAST classification. We evaluated plasma levels of IL-1beta, TNF-alpha, IL-6 and IL-10, E-selectin, P-selectin, sICAM-1,sVCAM-1, vWF, TPA and PAI-1. Patients with ischaemic stroke classified as cardio-embolic (CEI) showed, compared to other subtypes, significantly higher median plasma levels of TNF-alpha , IL-6 and IL-1beta. Furthermore stroke patients classified as lacunar showed, compared to other subtypes, significantly lower median plasma levels of TNF-alpha, IL-6 and IL-1beta. Multiple linear regression showed a significant association between the Scandinavian Stroke Scale (SSS) score at admission and diagnostic subtype, infarct volume of cardio-embolic strokes and some inflammatory variables. Our findings confirm that cardio-embolic strokes have a worse clinical presentation and produce larger and more disabling strokes than other ischaemic stroke subtypes reporting a possible explanation of higher immuno-inflammatory activation of the acute phase. Comment in Inflammatory markers for ischaemic stroke. [Thromb Haemost. 2009

Artificial Intelligence for Classifying the Relationship between Impacted Third Molar and Mandibular Canal on Panoramic Radiographs

The purpose of this investigation was to evaluate the diagnostic performance of two convolutional neural networks (CNNs), namely ResNet-152 and VGG-19, in analyzing, on panoramic images, the rapport that exists between the lower third molar (MM3) and the mandibular canal (MC), and to compare this performance with that of an inexperienced observer (a sixth year dental student). Utilizing the k-fold cross-validation technique, 142 MM3 images, cropped from 83 panoramic images, were split into 80% as training and validation data and 20% as test data. They were subsequently labeled by an experienced radiologist as the gold standard. In order to compare the diagnostic capabilities of CNN algorithms and the inexperienced observer, the diagnostic accuracy, sensitivity, specificity, and positive predictive value (PPV) were determined. ResNet-152 achieved a mean sensitivity, specificity, PPV, and accuracy, of 84.09%, 94.11%, 92.11%, and 88.86%, respectively. VGG-19 achieved 71.82%, 93.33%, 92.26%, and 85.28% regarding the aforementioned characteristics. The dental student's diagnostic performance was respectively 69.60%, 53.00%, 64.85%, and 62.53%. This work demonstrated the potential use of deep CNN architecture for the identification and evaluation of the contact between MM3 and MC in panoramic pictures. In addition, CNNs could be a useful tool to assist inexperienced observers in more accurately identifying contact relationships between MM3 and MC on panoramic images

Effects of clinical and laboratory variables and of pretreatment with cardiovascular drugs in acute ischaemic stroke: a retrospective chart review from the GIFA study.

Background: Few studies have examined the role of cardiovascular drugs on acute ischaemic stroke prognosis. Aims: To evaluate the relationship between a favourable outcome in patients with acute ischaemic stroke and specific demographic, clinical and laboratory variables and cardiovascular drug pretreatment. Methods: The 1096 patients enrolled in the GIFA study (who had a main discharge diagnosis of ischaemic stroke) represent the final patient sample used in this analysis. Drugs considered in the analysis included angiotensin converting enzyme (ACE)-inhibitors, angiotensin II receptor blockers, statins, calcium channel blockers, anti-platelet drugs, vitamin K antagonists and heparins. The outcomes analyzed included in-hospital mortality, cognitive function evaluated by the Hodkinson Abbreviated Mental Test (HAMT), and functional status evaluated by activities of daily living (ADL). The definition of a good outcome was no in-hospital mortality, a HAMT score of >= 6 and no ADL impairment. Results: Patients with no in-hospital mortality, a HAMT score of >6 and no ADL impairment were more likely to be younger at baseline and have a lower blood glucose level and a systolic blood pressure (SBP) between 120 and 180 mmHg, a higher plasma total cholesterol level, a lower white blood cell count, and a lower Charlson Index (CI) score, a higher rate of pretreatment with ACE-inhibitors, calcium channel blockers and a lower rate of pretreatment with heparin. Conclusions: Predictors of good outcome, in terms of in-hospital mortality and cognitive and functional performance at discharge, included higher SBP at admission between 120 and 180 mmHg, a SBP plasma total cholesterol levels, a lower CI score, and pretreatment with ACE-inhibitors, calcium channel blockers and anti-platelets. (C) 2010 Elsevier Ireland Ltd. All rights reserved