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The hide and viscera of cattle entering a slaughter facility are potential sources of contamination of carcasses including significant pathogens such as Escherichia coli O157:H7, Campylobacter spp. and Salmonella spp. If evisceration is correctly performed, visceral contents do not therefore contribute significantly to the overall contamination of the carcass. However, it is much more difficult to restrict contamination from the hide. The aim of this work is to investigate the relationships between the levels of dirt and contamination on the hide of animals presented for slaughter and the levels of contamination on the resultant carcasses. Cattle were visually inspected in the lairage of 2 abattoirs and assigned to a category ranging from 1 (very clean) to 5 (very dirty) depending on the observed cleanliness of the hide. Samples of hides and carcasses were taken from 50 animals for enumerate total viable counts, Enterobacteriaceae and Escherichia coli. The results show that there is a direct correlation between animal dirtiness and total bacterial count of the carcasses.

The quick enforcement of the RASFF is a key factor in minimizing possible threats to the consumers’, caused by the presence of foods jeopardizing animal/human health, or the environment. The Authors’ task is the design of some effectivness indicators for assessing the System’s information flow, focusing on timing; this would allow the definition of a benchmark for evaluating RASFF stakeholders’contribution.

The Authors studied physicochemical properties (pH and Aw) of samples of Nigiri sushi and their ingredients along their shelf life, integrating those results with a predictive microbiological model, in order to determine or to rule out the growth of Listeria monocytogenes above the thresholds set by Reg.(EU) 2073/2005. Results point towards substantial containment of the target biological hazard, even though the prevention of thermal abuse is a keypoint in increasing safety.

Foodborne pathogens including Escherichia coli O157:H7, Salmonella spp. and Campylobacter spp., can enter the meat chain at multiple points. Animals with excessively dirty hides will represent a risk of cross-contaminations during transport, in the slaughtered house environment and during dressing procedures. The aim of this work was to investigate the relationship among hygiene indicator microorganisms (Enterobacteriaceae and Escherichia coli) count, in hide and carcass of cattle presented for slaughter, and different hide cleanliness level in two abattoir (R and F) and estimate the prevalence of pathogens Escherichia coli O157:H7, Salmonella spp and Campylobacter spp. in hide and carcass of dirty animals. The results showed that hide Escherichia coli and Enterobacteriaceae count were significantly higher in dirty animals than in clean animals (P

First Codex Alimentarius, in international field, then EC Regulation 853/2004 ensure that animals that have such hide, skin or fleece conditions that there is an unacceptable risk of contamination of the meat during slaughter are not slaughtered for human consumption unless they are cleaned beforehand. In order to comply with such provisions, the operators must ensure that proper procedures have been fixed; the evaluation of such procedures is a priority for the Official Vet who must define standards of cleanliness. The authors take into account three different guidance schemes from Belgian and UK Food Safety Authorities and from the French Institut de l’Élevage in order to better classify cattle cleanliness at slaughter.

Inflammatory mechanisms play a pivotal role in the atherosclerotic process. At the base of atherogenesis there are complex interactions between macrophages, T lymphocytes and smooth muscle cells. A growing body of experimental evidences suggest that inflammation is involved in the pathogenesis of acute coronary syndromes (ACS) and influences their clinical evolution. In fact, in patients with ACS, coronary atherosclerotic plaques are characterized by an abundant inflammatory infiltrate. Moreover, in these patients systemic signs of inflammatory reaction can be observed: activated circulating inflammatory cells (neutrophil, monocytes and lymphocytes) and increased concentrations of pro-inflammatory cytokines, such as interleukin (IL)-1 and 6, and of acute phase reactants, in particular C-reactive protein (CRP). Recent data demonstrate that CRP is a strong independent predictor of adverse cardiac events and death in patients with ACS, but also in patients with stable ischemic heart disease and in apparently healthy men and women. Furthermore, CRP is an important prognostic index, for early and late outcome, in patients undergoing percutaneous coronary interventions, and may be useful in choosing the therapeutic management of the patient. Although the causes of inflammation in patients with ACS are not yet clear, this new line of research may open the way to a different clinical approach for these patients.

Inflammatory mechanisms and infectious agents, in association with "classic" cardiovascular risk factors, may be involved in the development of coronary atherosclerosis; moreover, recent studies demonstrated a direct role of inflammation in the pathogenesis of acute coronary syndromes, in which the intensity of the individual response to potential environmental inflammatory stimuli seems to influence the magnitude of the inflammatory reaction and the clinical outcome. The variability of this response may be modulated by genetic determinants, in particular by functional polymorphisms of the genes codifying for molecules involved in the inflammatory process. In this review we discuss the association between these polymorphisms and various aspects of ischemic heart disease. Although the association between this syndrome and genetic factors may be confounded by several elements (variable penetrance, different prevalence in different populations and age groups, interaction with environmental risk factors), presently available findings suggest that the inflammatory process in ischemic heart disease might be, at least in part, genetically mediated.

In order to evaluate whether different clinical presentations of unstable angina are associated with a different degree or pattern of activation of the hemostatic, fibrinolytic and inflammatory systems, we measured plasma levels of thrombin-antithrombin III, plasmin-alpha2- antiplasmin complexes and C-reactive protein, as markers of activation of coagulation, fibrinolysis and inflammation respectively, in two groups of patients: 7 patients with de novo unstable angina (Group 1) and 7 patients with destabilizing unstable angina (Group 2). Blood samples were taken on admission for measuring levels of C-reactive protein and during ischemic episodes at the onset of ECG changes and pain (0 min) and after 5, 15 and 60 min in order to assess the peak values of thrombin-antithrombin III and plasmin-alpha2-antiplasmin during the episode. Thrombin-antithrombin III levels in Group 1 were 1.8 microgram/l (0.3-4.15) at 0 min and increased to 17 micrograms/l (2.8-60) after 5 to 15 min (p = 0.013); conversely thrombin-antithrombin III levels in Group 2 were 2.15 microgram/l (1.4-3.8) at 0 min and raised to 4 micrograms/l (2-43) after 5 to 15 min (NS). No significant differences in both groups were observed in plasmin-alpha2-antiplasmin levels (Group 1:650 micrograms/l, ranged 492-956, at 0 min vs 670 microgram/l, range 415-977, at peak; Group 2: 480 micrograms/l, range 274-955, at 0 min vs 502 micrograms/l, range 304-1027, at peak; NS). Inversely, C-reactive protein levels on admission were 4 mg/dl (range 2-27) in Group 1, and 1 mg/dl (range 0.6-4) in Group 2 (p = 0.006). In conclusion, patients with de novo unstable angina have significantly enhanced thrombin (but not plasmin) production during spontaneous ischemic episodes than patients with destabilizing unstable angina. Furthermore, patients with de novo unstable angina have enhanced acute phase responses than patients with destabilizing unstable angina. Our data suggest that different pathogenetic mechanisms may be responsible for acute ischemic episodes in unstable angina and may explain different response to antithrombotic therapy in unstable angina patients.

Activated mast cells are present in human coronary atheromas, as well as in the adventitia of patients with variant angina, and may play an important role in plaque rupture and coronary vasomotion. To assess whether or not activation of mast cells is a primary event, we measured serum levels of tryptase, a specific marker of mast cell activation, in 8 patients with unstable angina during a spontaneous ischemic episode (Group 1) and in 5 patients with variant angina (Group 2) during ergonovine-induced coronary spasm. Blood samples were collected as soon as possible after the onset of pain and ECG changes (0 min), and after 5, 15 and 60 min. Tryptase levels in Group 1 were 0.13 U/l (range 0.017-0.44) at the onset of pain and significantly raised to 0.75 U/l (range 0.05-2.49) at 5 min, decreasing to 0.076 U/l (range 0.018-0.16) at 15 min and to 0.085 U/l (range 0.01-0.25) at 60 min (p = 0.035). Conversely, tryptase levels in Group 2 were 0.09 U/l (range 0.07-0.13) at 0 min, 0.11 U/l (range 0.07-0.22) at 5 min, 0.10 U/l (range 0.07-0.18) at 15 min, 0.11 U/l (range 0.07-0.17) at 60 min (NS). In conclusion, tryptase levels raise during spontaneous ischemic episodes in unstable angina, but not after ergonovine-provoked ischemia in variant angina, suggesting that a primary, yet unknown stimulus, may activate mast cells during some ischemic episodes in unstable angina.

Until a few years ago coronary atherosclerosis was thought to be a slowly progressive disease eventually leading to total coronary occlusion and myocardial infarction. Recent angiographic studies have shown, instead, that mild or moderate coronary stenoses have the highest risk of causing acute coronary syndromes when complicated by thrombus formation which, in turn, appears to be due to a complex interaction between the atherosclerotic background and acute ischemic stimuli. The tendency of the atherosclerotic background to develop thrombosis may be different in different patients, as indicated by the observation that the risk factor profile of patients who present with chronic coronary syndromes is different from that of patients who present with acute syndromes. The acute ischemic stimuli so far identified are: a sudden local thrombogenic stimulus; a transient systemic increase in systemic pro-coagulant activity; a transient increase in proximal and/or distal coronary tone. The recent observation of inflammatory cells activation, including T-lymphocytes, in patients with acute ischemic syndromes raises the intriguing possibility that a specific antigenic stimulus may play an important pathogenetic role.

The aim of this study was to provide a further contribution to the study on the alterations of left ventricular diastolic function induced by dialysis, using simple indexes of diastolic function obtained with Doppler. The study is conduced in 15 patients with renal failure aged between 22 and 51 years old by means of echocardiography M-2D a pulsed Doppler analysis of the left ventricular refilling flow, evaluated before and after dialysis. By the results is risen up that the dLA has had a significant reduction (p = 0.032), the dSLV have undergone a reduction that is not being significant, while the dDLV has had a significant reduction (p = 0.029), shortening fraction is improved even if in a not significant manner. Also the Doppler indexes has had a behaviour homogeneous in the group of studied patients. Early ventricular refilling is reduced, as showed by the reduction of E, consequence of the reduction preload, while the diastolic late refilling has showed a little increment, expressed by the increase af the peak A. The variations of these indexes, even if not statistically significant, express an alteration of pattern diastolic Doppler caused by both the reduction of preload and the alteration of ventricular relaxation. Besides this alteration, to our notice, is not to consider expression of myocardial compromise in this group studied patients. It would be however useful enlargement of the study to greater number of patients with follow-up for better comprehension of this cardiopathy and makes a more individual treatment of these patients.