New records of Malus crescimannoi (Rosaceae) in Sicily

New findings for Malus crescimmanoi, originally known from the mountain area near Floresta (Nebrodi Mts.). The new sites fall in Madonie Mts., where the species is found at the edge of Quercus petraea (Matt.) Liebl. and Fagus sylvatica woods, growing on quartzarenitic substratum at 1200-1800 m of elevation. These new localities are placed at the south-western limit of Fagus sylvatica distribution area, on both north-facing [Contrada Sempria (Castelbuono) and slopes of Madonna dell\u2019Alto (Castellana Sicula)], and south-facing slopes [Locality Prato (Polizzi Generosa)]

Evaluation of municipal waste incineration impact on environmental noise

The EU Directive 2002/49/EC or Environmental Noise Directive (END) aims to define a common approach intended to avoid, prevent or reduce the harmful effects, including annoyance, due to exposure to environmental noise. Under this Directive, member states are obliged to produce the noise maps of the major roads, railways airports, large agglomerations and industrial activity sites. The first maps had to be produced for the main agglomerations by July 2007 and the first action plans should be activated no lather than July 2008. In this work we consider the industrial noise produced by municipal waste incineration; the study was developed to provide data of the sound power level along the facades buildings and contours of this site that can be used to produce strategic noise maps. To characterize the impact of the waste incineration plant, measurements of the noise emissions were performed in situ. The distribution of sound power and sound input levels have been calculated by SoundPLAN\uae computer model. The results of this work can provide a re-applicable method for the production of noise levels due to industrial noise sources. The results are suitable to be included in noise maps for agglomerations, in line with the END expectatio

Effects of ACE-inhibitors and angiotensin receptor blockers on inflammation.

The role of inflammation in cardiovascular disease and in hypertensive disease above all, is complex. Several studies confirm that activation of renin-angiotensin-aldosterone system (RAAS), through increase in the production of angiotensin II (Ang II), is closely related to local vascular inflammation. Over the BP lowering effects of anti-hypertensive treatments, several ancillary effects for every class may be found, distinguishing the various drugs from one another. Given the pro-inflammatory effects of Ang II and aldosterone, agents that interfere with the components of RAAS, such as ACE inhibitors, Angiotensin Receptor Blockers (ARBs), and mineralocorticoid receptor antagonists (spironolactone or the more selective eplerenone), represent logical therapeutic tools to reduce vascular inflammation and cardiovascular risk, as suggested in large clinical trials in patients with hypertension and diabetes. Regarding ACE inhibitors, actually there is no convincing evidence indicating that ACEi's reduce plasma levels of major inflammatory markers in hypertension models. Lack of evidence concerns especially these inflammation markers, such as fibrinogen of CRP, which are less closely related to atherosclerotic disease and vascular damage and conversely are affected by several more aspecific factors. Results obtained by trials accomplished using ARBs seem to be more univocal to confirm, although to great extent, these is an anti-inflammatory effect of drugs blocking AT1 receptor. In order to strictly study the effects of blockage of RAAS on inflammation, future studies may explore different strategies by, for example, simultaneously acting on the ACE and the AT1 angiotensin receptors

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

Antivitamin K drugs in stroke prevention.

Among the different subtypes of ischaemic strokes, almost 20 % are of cardiac origin. Different are the causes of cardioembolic stroke, but the most common is the atrial fibrillation, a supraventricular arrhythmia. Appropriate use of antiplatelet drugs and anticoagulants after transient ischaemic attack (TIA) or ischaemic stroke depends on whether the underlying cause is cardioembolic or of presumed arterial origin. Adequate antiplatelet therapy is recommended for secondary prevention after cerebral ischaemia of presumed arterial origin, whether for patients with TIA and ischaemic stroke of cardiac origin, mainly due to atrial fibrillation. Vitamin K antagonists (VKAs) are highly effective in preventing recurrent ischaemic stroke but have important limitations and are thus underused. Current guidelines still regard Vitamin K Antagonists at INR 2·0-3·0 to be the standard treatment after cerebral ischaemia of cardiac origin for patients who can tolerate them. In this setting antiplatelet therapy provides an alternative when oral anticoagulation is contraindicated or when patient choice or compliance limits choice of therapy, but is much less effective than VKAs. Recent trial data performed with new anticogulants such as the factor Xa and thrombin inhibitors will need to be taken into account, in order to prevent several of the clinical problems actually related to VKAs use

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

Arterial stiffness and ischemic stroke in subjects with and without metabolic syndrome.

We conducted a study to evaluate arterial stiffness markers in subjects with acute ischemic stroke and metabolic syndrome and in relation to TOAST subtype of stroke. We enrolled 130 patients with acute ischemic stroke and metabolic syndrome, 127 patients with acute ischemic stroke without metabolic syndrome and 120 control subjects without acute stroke. Applanation tonometry to record pulse wave velocity (PWV). Stroke patients with metabolic syndrome, compared control subjects without stroke showed higher PWV. In subjects with ischemic stroke and metabolic syndrome, PWV was more significantly and positively correlated with body mass index, systolic blood pressure, hypertension, diabetes, glucose blood levels, LDL cholesterol levels, total cholesterol levels, micro-albuminuria, carotid plaque, previous brain infarct at neuro-imaging. Our findings underline important role of both small vessel disease and atherosclerosis on arterial stiffness pathogenesis in the clinical setting of metabolic syndrom

BCR-ABL1 doubling-times and halving-times may predict CML response to tyrosine kinase inhibitors

In Chronic Myeloid Leukemia (CML), successful treatment requires accurate molecular monitoring to evaluate disease response and provide timely interventions for patients failing to achieve the desired outcomes. We wanted to determine whether measuring BCR-ABL1 mRNA doubling-times (DTs) could distinguish inconsequential rises in the oncogene’s expression from resistance to tyrosine kinase inhibitors (TKIs). Thus, we retrospectively examined BCR-ABL1 evolution in 305 chronic-phase CML patients receiving imatinib mesylate (IM) as a first line treatment. Patients were subdivided in two groups: those with a confirmed rise in BCR-ABL1 transcripts without MR3.0 loss and those failing IM. We found that the DTs of the former patients were significantly longer than those of patients developing IM resistance (57.80 vs. 41.45 days, p = 0.0114). Interestingly, the DT values of individuals failing second-generation (2G) TKIs after developing IM resistance were considerably shorter than those observed at the time of IM failure (27.20 vs. 41.45 days; p = 0.0035). We next wanted to establish if decreases in BCR-ABL1 transcripts would identify subjects likely to obtain deep molecular responses. We therefore analyzed the BCR-ABL1 halving-times (HTs) of a different cohort comprising 174 individuals receiving IM in first line and observed that, regardless of the time point selected for our analyses (6, 12, or 18 months), HTs were significantly shorter in subjects achieving superior molecular responses (p = 0.002 at 6 months; p < 0.001 at 12 months; p = 0.0099 at 18 months). Moreover, 50 patients receiving 2G TKIs as first line therapy and obtaining an MR3.0 (after 6 months; p = 0.003) or an MR4.0 (after 12 months; p = 0.019) displayed significantly shorter HTs than individuals lacking these molecular responses. Our findings suggest that BCR-ABL1 DTs and HTs are reliable tools to, respectively, identify subjects in MR3.0 that are failing their assigned TKI or to recognize patients likely to achieve deep molecular responses that should be considered for treatment discontinuation