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Nocardia farcinica is a rare Nocardia species causing localised and disseminated infections. A case of Nocardia farcinica infection is presented, and 52 cases previously reported in the literature are reviewed. The hosts usually had predisposing conditions (85%), and acquired the infection through the respiratory tract or skin; the infection then often spread to the brain, kidney, joints, bones and eyes. Pulmonary or pleural infections (43%), brain abscesses (30%) and wound infections (15%) which failed to respond to conventional antimicrobial therapy were the more frequent forms of infection. Nocardia farcinica was frequently isolated from pus (100% of samples), bronchial secretions (41%) and biopsy specimens (63%), but isolation from blood and urine, as in the case presented here, is rare. Antibiotic therapy was adequate in 61% of the patients in whom it was specified, the agents most frequently given being trimethoprim-sulfamethoxazole (54%), amikacin combined with imipenem (7%) and amoxicillin-clavulanate (7%). The high mortality (31%) can be attributed to the severe underlying diseases present, difficulties encountered in identifying the pathogen, inappropriate therapy and late initiation of therapy. Although an infrequent pathogen, Nocardia farcinica should be kept in mind as a cause of infection especially in immunosuppressed patients with indolent infections not responding to third-generation cephalosporins.

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Ischemia-modified albumin (IMA) has been proposed as a biological marker of myocardial ischemia (1, 2 ). Exposure to ischemic myocardium modifies circulating albumin at its NH 2 terminus by different mechanisms, and this modification is the basis of IMA measurement by the albumin cobalt binding (ACB) test (3 ). The tissue-specific nature of the mechanism by which ischemia modifies albumin remains undetermined. Together with a nondiagnostic electrocardiogram and negative troponin values, IMA concentrations within the reference interval have high negative predictive value of myocardial ischemia in patients with suspected acute coronary syndromes (1, 2 ). However, IMA cardiospecificity has not been validated and needs an evidence base before routine clinical use. A recent report showed significant IMA increases 24 -48 h after a marathon race, with exercise-promoted gastrointestinal and/or delayed skeletal muscle ischemia being evoked as possible causes of such increases (4 ). However, because IMA has shown rapid kinetics of increase (in minutes) and return to baseline no longer than 12 h after angioplastic procedures (5 ), long-duration skeletal muscle ischemia (i.e., occurring during marathons) does not appear to be the most appropriate model to investigate the effect of such ischemia on IMA values or the kinetics of IMA occurring during acute coronary syndromes. The aim of this work was to analyze the possible contribution of skeletal muscle ischemia to IMA by investigating its short-term kinetics in an isolated skeletal-muscle ischemia model. Because lactate and ammonia concentrations increase sharply after a forearm ischemia test, their possible influence in the ACB assay was studied.Ten healthy volunteers (4 men and 6 women) from our laboratory staff (age range, 48 -61 years; median, 53 years) with no personal or family history of cardiovascular disease and no known cardiovascular risk factors after a medical examination underwent a forearm ischemia test (6 ). Briefly, after an overnight fast (10 -12 h) and 30 min of previous rest, a preexercise (0 min) blood sample was drawn, and blood systolic pressure was recorded twice within a 5-min interval. Thereafter, forearm ischemia was produced by inflating the blood pressure cuff up to 20 -30 mmHg higher than the maximum systolic pressure registered. Under these ischemic conditions, a hand-grip exercise at maximum possible strength was performed for 1 min. Thereafter, the cuff was removed, and serial blood samples were drawn at 1, 3, 5, 10, 15, and 30 min. Serum for IMA, creatine kinase, and potassium; EDTA plasma for ammonia; and fluoride plasma for lactate and glucose were collected at each time point into Vacutainer ® Tubes (Becton Dickinson). To establish reference values, IMA was tested in a group of 86 fasting (10 -12 h), ambulatory (median age, 57 years; 38 women) sedentary individuals who underwent blood sampling after health examinations or before minor surgical procedures. Individuals with cardiovascular risk factors or past or present signs or symptoms o...

The forecast f o r the year 2000 indicates a need to produce 164Experiments were conducted to measure the influence of the main variables in protein extraction (concentration, temperature, time, solid/liquid ratio and pH). Sodium hydroxide, sodium chloride and magnesium chloride aqueous solutions (of different ionic strength) and de-ionised water were used as extracting solvents.The results are reported in Table 1. In general, the most efficient extracting solution was aqueous NaOH. The water-extracted protein amounts were higher than those in salt solutions, as observed by Castriotta and Canella (1978) in Italian grapeseeds. Table 1 clearly shows that increasing ionic strength reduces the protein extractability, which is considerably lower in MgCl, solutions than in NaCl solutions. In addition, it seems that concentrations above 0

Atrial fibrillation (AF) has been associated with increased spontaneous calcium release from the sarcoplasmic reticulum and linked to increased adenosine A2A receptor (A2AR) expression and activation. Here we tested whether this may favor atrial arrhythmogenesis by promoting beat-to-beat alternation and irregularity. Patch-clamp and confocal calcium imaging was used to measure the beat-to-beat response of the calcium current and transient in human atrial myocytes. Responses were classified as uniform, alternating or irregular and stimulation of Gs-protein coupled receptors decreased the frequency where a uniform response could be maintained from 1.0 ± 0.1 to 0.6 ± 0.1 Hz; p < 0.01 for beta-adrenergic receptors and from 1.4 ± 0.1 to 0.5 ± 0.1 Hz; p < 0.05 for A2ARs. The latter was linked to increased spontaneous calcium release and after-depolarizations. Moreover, A2AR activation increased the fraction of non-uniformly responding cells in HL-1 myocyte cultures from 19 ± 3 to 51 ± 9 %; p < 0.02, and electrical mapping in perfused porcine atria revealed that adenosine induced electrical alternans at longer cycle lengths, doubled the fraction of electrodes showing alternation, and increased the amplitude of alternations. Importantly, protein kinase A inhibition increased the highest frequency where uniform responses could be maintained from 0.84 ± 0.12 to 1.86 ± 0.11 Hz; p < 0.001 and prevention of A2AR-activation with exogenous adenosine deaminase selectively increased the threshold from 0.8 ± 0.1 to 1.2 ± 0.1 Hz; p = 0.001 in myocytes from patients with AF. In conclusion, A2AR-activation promotes beat-to-beat irregularities in the calcium transient in human atrial myocytes, and prevention of A2AR activation may be a novel means to maintain uniform beat-to-beat responses at higher beating frequencies in patients with atrial fibrillation.

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Atrial fibrillation (AF) is the most common form of cardiac arrhythmia seen in clinical practice. While some clinical parameters may predict the transition from paroxysmal to persistent AF, the molecular mechanisms behind the AF perpetuation are poorly understood. Thus, oxidative stress, calcium overload and inflammation, among others, are believed to be involved in AF-induced atrial remodelling. Interestingly, adenosine and its receptors have also been related to AF development and perpetuation. Here, we investigated the expression of adenosine A2A receptor (A2AR) both in right atrium biopsies and peripheral blood mononuclear cells (PBMCs) from non-dilated sinus rhythm (ndSR), dilated sinus rhythm (dSR) and AF patients. In addition, plasma adenosine content and adenosine deaminase (ADA) activity in these subjects were also determined. Our results revealed increased A2AR expression in the right atrium from AF patients, as previously described. Interestingly, increased levels of adenosine content and reduced ADA activity in plasma from AF patients were detected. An increase was observed when A2AR expression was assessed in PBMCs from AF subjects. Importantly, a positive correlation (P=0.001) between A2AR expression in the right atrium and PBMCs was observed. Overall, these results highlight the importance of the A2AR in AF and suggest that the evaluation of this receptor in PBMCs may be potentially be useful in monitoring disease severity and the efficacy of pharmacological treatments in AF patients.