OBJECTIVE -Stress hyperglycemia has been associated with increased mortality in patients with myocardial infarction (MI). We examined the association between plasma glucose levels, circulating inflammatory markers, T-cell activation, and functional cardiac outcome in patients with first MI. RESEARCH DESIGN AND METHODS -Echocardiographic parameters, circulating levels of interleukin-18 (IL-18), C-reactive protein (CPR), and the percent of CD16-CD56, CD4/CD8, CD152, and HLA-DR expression were investigated in 108 patients with acute MI on admission to the emergency ward.RESULTS -Our review found that 31 new hyperglycemic patients (glycemia Ն7 mmol/l) had higher infarct segment length (P Ͻ 0.05) and myocardial performance index (P Ͻ 0.02) and reduced transmitral Doppler flow (P Ͻ 0.05), pulmonary flow analysis (P Ͻ 0.02), and ejection fraction (P Ͻ 0.05) compared with 36 hyperglycemic diabetic patients and 41 normoglycemic patients. Plasma IL-18 and CRP were higher in the hyperglycemic than in the normoglycemic patients (P Ͻ 0.005), with the highest values in patients with new hyperglycemia (P Ͻ 0.05). Hyperglycemic patients had a higher percent of CD16ϩ/CD56ϩ cells and CD4/CD8 ratio (P Ͻ 0.01), whereas they had lower CD152 expression (which has a negative regulatory function in T-cell activation) compared with normoglycemic patients (P Ͻ 0.001).CONCLUSIONS -During MI, hyperglycemia is associated with increased levels of inflammatory markers, enhanced expression of cytotoxic T-cells, and reduced expression of T-cells, which are implicated in limiting the immune process. An increased inflammatory immune process seems a likely mechanism linking acute hyperglycemia to poor cardiac outcome in MI patients. Diabetes Care 26:3129 -3135, 2003A n unusually high prevalence of glycosuria in nondiabetic patients who have acute myocardial infarction (MI) was noted as early as 1931 (1). Stress hyperglycemia after MI is associated with an increased risk of in-hospital mortality in patients with and without diabetes (2). Moreover, a positive association between hyperglycemia at the time of the event and subsequent mortality from MI has been reported (3). Although the mechanisms underlying this association are not fully understood, evidence that the use of insulin to lower glucose concentrations decreases mortality in diabetic patients who have MI (4) suggests that hyperglycemia is not simply an epiphenomenon of a stress response. Consequently, hyperglycemia at the time of MI may be an important and potentially modifiable risk factor for poor outcome.A growing body of evidence suggests that MI is associated with local and systemic inflammation (5). Cell activation, which is mediated to some extent by immune mechanisms, is an important component of inflammatory reaction (6). Atherosclerotic plaques contain large numbers of activated T-cells, suggesting that immune mechanisms are important factors in the pathogenesis of the atherosclerotic background (6). Indeed, inflammatory cells infiltrate nearly all plaques, and culprit lesions of...

A colorimetric MTT (tetrazolium salt) cleavage test was used to evaluate cytotoxicity of twenty-three Fusarium mycotoxins on two cultured human cell lines (K-562 and MIN-GL1) as well as their inhibitory effect on proliferation of phytohemagglutinin-stimulated human peripheral blood lymphocytes. The values of 50% inhibition of lymphocyte blastogenesis were very close to the 50% cytotoxic doses observed with the more sensitive cell line (MIN-GL1). T-2 toxin was the most cytotoxic with CD50 and ID50 values less than 1 ng/ml. Type A trichothecenes were the most cytotoxic followed by the type B trichothecenes; the non-trichothecenes were the least cytotoxic. The MTT cleavage test, in conjunction with cell culture, is a simple and rapid bioassay to evaluate cytotoxicity and immunotoxicity of Fusarium mycotoxins.

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Primary cardiac lymphoma (PCL), defined as a lymphoma clinically mimicking cardiac disease, with the bulk of the tumor located intrapericardially, is extremely rare in immunocompetent patients. Clinical manifestations vary depending on sites of involvement in the heart and include chest pain, arrhythmias, pericardial effusion, and heart failure. Diagnosis is often difficult and may require invasive procedures; in some cases, diagnosis is not made until autopsy. Histologically, nearly all cases of PCL reported thus far have been of B-cell origin. In this report, we describe a case of PCL of T-cell origin in an adult immunocompetent patient, the second reported in the literature to the best of our knowledge, and provide a brief overview of the features of previously published PCL cases.

Off-label omalizumab was safe and effective in our patients. The novel immunologic features recorded in our patients add further complexity to the mechanism of action of omalizumab.

CD4+CD25+Foxp3+ regulatory T cells (Treg) specialize in suppressing immune responses. In this study, 47 consecutive colon cancer patients were subjected to circulating Treg frequency assessment by flow cytometry before and after cancer resection. Thirty-two healthy subjects served as controls. Circulating Treg frequencies were significantly higher in colon cancer patients with respect to healthy controls. When patients were subgrouped according to Dukes stages, a linear relationship was observed between Dukes stages and Treg frequencies. In radically resected patients, Treg frequencies were shown to have significantly dropped down. Patients with advanced colon cancer were more likely to have significantly higher proportions of circulating Treg frequencies than Dukes A and B patients when compared to healthy subjects. Of note, nonradically resected patients were found to display reductions in-but not normalization of-Treg frequencies. These results suggest that cancer itself may be able to drive Treg recruitment as a strategy of immunoevasion.

. Vigorous exercise acutely changes platelet and B-lymphocyte CD39 expression. J Appl Physiol 98: 1414 -1419, 2005; doi:10.1152/japplphysiol.00315.2004.-CD39/ATP diphosphohydrolase is expressed on B lymphocytes, cytotoxic T lymphocytes, monocytes, platelets, and endothelial cells, and it has a critical role in the inhibition of platelet responsiveness. To determine whether strenuous exercise could acutely change expression of CD39 in platelets and lymphocytes, eight healthy sedentary men, 34 yr old (SD 7), and eight physically active men, 34 yr old (SD 6), performed graded upright cycle ergometry to volitional exhaustion. Blood samples collected both at baseline and after exercise test were employed to measure CD39 expression in platelets and lymphocytes. The percentage of circulating platelet-platelet aggregates, the "in vitro" ADP and collagen-induced platelet aggregation, and the expression of both platelet glycoprotein IIb-IIIa (PAC-1) and Pselectin (CD62) were also considered markers of platelet activation. After strenuous exercise, all subjects demonstrated significant platelet activation as judged by the increased percentage of platelet-platelet aggregates. The in vitro ADP-induced platelet aggregation and the expression of CD62P on ADP-stimulated platelets significantly increased in sedentary but not in active subjects. After exercise, all of the subjects showed a significant reduction of CD39 expression in platelet [sedentary: from 2.2 (SD 0.8) to 1.1% (SD 0.8), P ϭ 0.008; active: from 0.6 (SD 0.2) to 0.35% (SD 0.1), P ϭ 0.009] and an increase of CD39 expression in B lymphocytes [sedentary: from 47 (SD 13) to 60% (SD 11), P ϭ 0.0039; active: from 46 (SD 11) to 59% (SD 11), P ϭ 0.0038]. Taken together, these findings confirm the critical role of this ADPase in inhibition of platelet responsiveness, also suggesting a possible role of B lymphocytes in thromboregulation mechanism. sedentary men; active men; thromboregulation IN EPIDEMIOLOGICAL studies, moderate and vigorous exercise have been associated with a decrease in the risk of cardiovascular disease (1,16,27,41). However, vigorous exercise can acutely and transiently increase the risk of myocardial infarction and cardiac death, especially in sedentary subjects and in those with coronary heart disease (15, 31, 37, 43). The mechanism by which exercise triggers an acute cardiac event is not entirely known, although coronary thrombosis plays a key role. Several reports have demonstrated that strenuous exercise induces platelet activation, thus increasing thrombotic tendency (5,22,25,33,34). Various mechanisms, including increased plasma levels of norepinephrine and epinephrine (36), altered response of platelet ␣ 2 -adrenergic receptors (39), and impaired sensitivity of platelets to nitric oxide (NO) (34), have been hypothesized to explain both the increased platelet activation and reactivity after strenuous exercise. The role of hemoconcentration induced by acute exercise also has been considered (8, 40). The epidemiology of coronary artery disease indi...

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