SummaryBackground: Some patients evaluated for chest pain with angiographically normal coronary arteries show coronary slow flow phenomenon (CSFP) on angiography. Slow flow of dye in epicardial coronary arteries is also not an infrequent finding in patients during routine coronary angiography. The precise pathophysiology of CSFP is not known yet.Hypothesis: This study investigates the presence of platelet function disorders in patients with CSFP.Methods: The patient group included 24 patients with CSFP detected by coronary angiography via the TIMI "frame count" method, and a control group included 23 patients with normal coronary flow. Platelet aggregability induced by use of ristocetin, collagen, and adenosine diphosphate (ADP), was measured from all blood samples in both control and patient groups.Results: The ratio of platelet aggregability increased significantly in patients with CSFP compared with patients with normal coronary flow (ristocetin 57.6 ± 15 vs. 45.4 ± 17.1, collagen 62.9 ± 16.4 vs. 48.9 ± 25.3, ADP 59.4 ± 18 vs. 42.4 ± 15.2, p < 0.05).Conclusion: Platelet aggregability is increased in patients with CSFP.

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Heparin has an apoptotic effect beside its anticoagulant, anti-inflammatory, antihypertensive, and antiproliferative effects. In this study, the authors detected the percentages of apoptotic lymphoblasts and the expressions of apoptotic Fas protein and antiapoptotic Bcl-2 protein with flow cytometry in vitro after the incubation of lymphoblasts with heparin. Eleven newly diagnosed acute lymphoblastic leukemia (ALL) children were included in the study. Lymphoblasts were incubated in all different levels of heparin concentrations (0, 10, and 20 U/mL) and the percentages of apoptotic lymphoblasts and the percentages of Fas protein and Bcl-2 proteins were simultaneously measured by flow cytometry at 0, 1, and 2 h. At 0, 1, and 2 h, apoptosis was determined when heparin was added in 10- and 20-U/mL concentrations (p <.05). The apoptotic effect of heparin on lymphoblasts was higher at the first hour than at 0 and 2 h in 10- and 20-U/mL heparin concentrations (p <.01). The highest apoptosis was detected in the 20-U/mL heparin concentration at the first hour. The expression levels of Fas protein on lymphoblasts were higher at the first hour than at 0 and 2 h in 10- and 20-U/mL heparin concentrations (p <.001). The highest expression of Fas protein was observed in the 20-U/mL heparin concentration at the first hour. The expression levels of Bcl-2 protein on lymphoblasts were lower at the first hour than at 0 and 2 h in 10- and 20-U/mL heparin concentrations (p <.001). The lowest expression of Bcl-2 protein was detected in the 20-U/mL heparin concentration at the first hour. Increased concentrations of heparin had an increasing effect on the percentages of apoptotic lymphoblasts. The expression percentages of Fas protein on lymphoblasts also increased, whereas the expression percentages of Bcl-2 protein on lymphoblasts decreased (p <.05). These results suggest that low-dose heparin may cause significant apoptosis of lymphoblasts in newly diagnosed ALL patients.

Background/Aim: Pterygium is a relatively frequent ocular surface disease with an unexplained etiopathogenesis. Our study was carried out with the aim to identify the presence of inflammatory cells and mediators such as T-lymphocyte subgroups (CD4 and CD8), intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and human leukocyte antigen-DR (HLA-DR) in pterygium tissue. Methods: Pterygium tissue, obtained from 24 patients, and normal conjunctival tissue, from the nasal bulbar conjunctiva obtained from 14 patients operated for ocular perforations or vitrectomy, were separated into epithelial and stromal components under the microscope and suspended with phosphate-buffered saline solution to form a suspension. Cell suspensions were treated with specific antibodies for ICAM-1, VCAM-1, and HLA-DR and T-lymphocyte subgroups and evaluated with flow cytometry. The obtained data were compared statistically. Results: When compared to the control tissue samples, higher rates of ICAM-1-positive cells, VCAM-1-positive cells and HLA-DR-positive cells were recorded in pterygium tissue samples. CD4 and CD8 lymphocytes were also found to be at higher levels when compared to the control group. There was a statistically significant difference between the two groups. Conclusion: When compared with normal conjunctival tissue, pterygium tissue had increased levels of T-lymphocyte infiltration and inflammatory markers demonstrating the possible contribution of cellular immunity to the pathogenesis.

For oesophageal epithelial changes to develop from gastro-oesophageal reflux disease (GORD), the character of the refluxate must be acid enough to cause injury. Experimentally, copious perfusion of the oesophagus with weak acid is quite harmless. However, hydrochloric acid alone with a pH below 3.0 may cause oesophageal injury. Cola drinks are strongly acidic (pH 2.5). This study analyses the influence of and possible interaction between cola consumption and oesophagitis. Twenty rats were divided into two groups of 10. The animals received saline (pH 7.0) or cola (pH 2.6) per OS with 24 h free access to these solutions. After the experiment the oesophagus was dissected. The mucosa was macroscopically and histopathologically examined, and flow cytometric analysis was used to look for proliferative activity. The histopathological analysis showed that there is no difference between saline and cola. But the findings of cell cycle analysis showed that the effects of cola and saline in inducing oesophageal mucosal damage are different. In the cola group the values were G0/G1, 7.33 +/- 2.88; S, 29.88 +/- 2.88; G2/M, 0.10 +/- 0.01; PI (proliferative-regenerative index), 29.76 +/- 2.88. The rat cell population g0/g1 phases were found to be low (p < 0.01), and the cell population S and PI phases were found to be significantly elevated compared with the control group (p < 0.01). (G0/G1, 79.30 +/- 5.97; S, 16.06 +/- 8.27; G2/M, 4.66 +/- 4.03; PI, 20.03 +/- 6.01). These results were reflected in the proliferative index, which is used as a measure of the regeneration index. The data show that cola has proliferative and regenerative effects on the oesophageal mucosa, and it is possible that its regenerative effect is caused as a result of an irritant effect.

In this study the apoptotic effects of heparin on lymphoblasts, neutrophils, and mononuclear cells were evaluated by flow cytometry for detection of sub-G 1 peak, in vitro. Ten children with acute lymphoblastic leukemia (ALL) at diagnosis (Group I), six children with ALL at relapse (Group II), and 10 healthy children (controls) were included in this study. Lymphoblasts in ALL patients, and neutrophils and mononuclear cells in controls, were incubated in increasing heparin concentrations (0, 5, 10, 20 U/ml). Flow cytometric analyses were performed at 0, 1, and 2 hours of incubation in heparin for determination of the apoptotic effects of heparin. In Group I apoptosis was detected in all different levels of heparin concentration except 0 U/ml at 0, 1, and 2 hours. The apoptotic effects of heparin on blast cells peaked at the first hour in 5-, 10-, and 20-U/ml heparin concentrations (p < 0.0001). In Group II similar findings were observed only at zero hour and apoptosis was higher than those in Group I except in 5-U/ml heparin concentration (p < 0.001). Apoptosis was found to increase with heparin levels in both groups (p < 0.02). In the control group, apoptosis was detected only at the 20-U/ml heparin concentration and only at the first and second hours. Lymphoblasts are more sensitive to apoptotic effects of heparin than either neutrophils and mononuclear cells (p < 0.004). It can be suggested that low-dose heparin may cause significant apoptosis of lymphoblasts while inducing no apoptosis on neutrophils and mononuclear cells. The findings of this preliminary study indicate that further and more comprehensive research on the apoptotic effect of heparin on lymphoblasts should be done. Am. J. Hematol. 61:90-93, 1999.

The apoptotic effect of heparin on the lymphoblasts obtained from 12 newly diagnosed children with acute lymphoblastic leukemia (ALL) was investigated in vitro. The lymphoblasts were incubated with 0, 10, and 20 U/mL heparin concentrations at 0, 1, and 2 h. The percentages of the apoptotic lymphoblasts were calculated by flow cytometry (FCM), and activities of caspase-3 and -8 were simultaneously measured by fluorometric protease activity method. The apoptotic effect of heparin on the lymphoblasts was determined in 10 and 20 U/mL heparin concentrations (p < 0.005 and p < 0.001, respectively) while no apoptosis was detected in 0 U/mL heparin concentration at 0, 1, and 2 h. The apoptotic percentages of the lymphoblasts were higher at the first hour than those at 0 and 2 h in 10 and 20 U/mL heparin levels (p < 0.001). The highest apoptosis was found at first hour in 20 U/mL heparin concentration. Increased concentrations of heparin had an increasing effect on the percentages of the apoptotic lymphoblasts. Significantly higher caspase-3 and -8 activities were determined in 10 and 20 U/mL heparin concentrations than those in 0 U/mL heparin concentration at 0, 1, and 2 h (p < 0.001). There were no significant differences between the caspase-3 and -8 activities in 10 and 20 U/mL heparin concentrations at 1 and 2 h (p > 0.05), while statistically significant differences were simultaneously detected in the apoptotic rates of the lymphoblasts (p < 0.001). This may be due to that the study included the limited patients, or measurement of the caspase activities is a more sensitive method than the FCM analysis for determination of apoptosis because the activation time of the caspases takes a long time period. It was concluded that the apoptotic effect of heparin in vitro on lymphoblasts developed due to the extrinsic pathway of apoptosis via the caspase-3 and -8 activations in newly diagnosed ALL patients.