Expression and prognostic value of the Ki-67 in Wilms’ tumor: experience with 48 cases

Purpose  

Ki-67, tumor proliferation marker, is an important prognostic factor in a variety of cancers. In the present study, we investigated the expression and the prognostic value of Ki-67 in nephroblastoma.     

Extract of green tea leaves partially attenuates streptozotocin-induced changes in antioxidant status and gastrointestinal functioning in rats

Rats with severe streptozotocin (STZ)-induced diabetes were subjected to dietary green tea extract supplementation at 2 doses (0.01% and 0.2%; GTL and GTH groups, respectively) to evaluate their effects on antioxidant, gastrointestinal, and renal parameters of experimental animals. The lower dietary supplementation reflects daily consumption of 3 cups of green tea for an average adult weighing 70 kg. Supplementation of a diet with green tea extract had no influence on elevated food intake, body weight loss, increased glucose concentration, or declined antioxidant capacity of water-soluble substances in plasma in the diabetic rats. In cases of intestinal maltase activity, attenuation of liver and kidney hypertrophy, triacylglycerol concentration, and aspartate aminotransferase activity in the serum, both dietary treatments normalized metabolic disorders caused by STZ injection to a similar extent. Unlike the GTL group, the GTH treatment significantly ameliorated development of diabetes-induced abnormal values for small intestinal saccharase and lactase activities, renal microalbuminuria, thiobarbituric acid-reactive substance content in kidney tissue, as well as total antioxidant status in the serum of rats. The GTH group was also characterized by higher antioxidant capacity of lipid-soluble substances in plasma and superoxide dismutase activity in the serum. Although the higher dose of green tea extract did not completely protect against STZ-induced hyperglycemia and oxidative stress in experimental rats, this study suggests that green tea extract ingested at high amounts may prove to be a useful therapeutic option in the reversal of diabetic dysfunction.     

Effect of allergen-specific immunotherapy on platelet secretory activity in patients with grass-pollen allergy

Platelet may become activated following antigen challenge to participate then actively in the immune-inflammatory response. Moreover, some evidence proves that specific immunotherapy induces changes in the platelet function. The objective of this study was to determine circulating platelet activity during the early phase of allergen-specific immunotherapy (SIT) in patients with grass pollen-sensitive allergic rhinitis. Twelve grass-pollen allergic patients (seven men and five women) with intermittent allergic rhinitis were treated with specific subcutaneous allergoid preparation. SIT was received by six weekly injections, the vaccine dose increasing until the maintenance level was reached. Blood was sampled at four different time points: before and directly before SIT, 30 min and 24 h after the maximum dose injection of the vaccine. Plasma level of beta-thromboglobulin (beta-TG), marker of platelet activation in vivo was measured using ELISA method. Baseline beta-TG level did not differ significantly among the patients and healthy subjects. Moreover, no significant differences were observed in the degree of platelet activity between the different times of this study in the patients group. We failed to detect any significant changes in circulating platelet activity, the measure of plasma level of beta-TG, in patients with grass-pollen induced intermittent rhinitis during the course of the dose increase phase of grass pollen SIT. In particular, it seems that both early (after 30 min) and late (after 24 h) changes in plasma level of this marker do not occur following the maximum dose administration of the allergen vaccine during the early SIT phase.     

The Effects of Raloxifene and Simvastatin on Plasma Lipids and Endothelium

Purpose: Raloxifene is a selective estrogen receptor modulator and an attractive alternative to estrogen replacement as it obviates the need for a progestin and does not increase C-reactive protein levels. We compared the effects of simvastatin and raloxifene treatments on the lipid profile, the levels of adhesion molecules and the endothelium dependent and independent vasoreactivity. Subjects & Methods: We treated 12 postmenopausal women with hypercholesterolemia and coronary artery disease with raloxifene 60 mg/day and simvastatin 20 mg/day in a randomized, double-blind, crossover study. Each treatment period was 8 weeks long with a 4-week washout interval. Plasma lipids and cellular adhesion molecules were evaluated and peripheral blood flow studies with venous occlusion plethysmography were performed. Results: Both simvastatin and raloxifene significantly reduced total [33% (27–40), 12% (0–24)] and LDL [44% (36–52), 16% (0–33)] cholesterol compared to baseline values (p < 0.05) but simvastatin was more effective than raloxifene (p < 0.005). None of the treatments had any significant effect on HDL cholesterol and triglyceride levels. Only raloxifene significantly reduced Lp(a) [18% (1–36)] and ICAM-1 [17% (8–25)] and VCAM-1 [24% (15–33)] plasma levels compared to baseline (p = 0.019, p < 0.0001 and p = 0.003, respectively). Hyperemic blood flow response on raloxifene was significantly higher compared to baseline [52% (0–105)], (p < 0.05), whereas no significant change was noted on simvastatin. Endothelium independent blood flow induced by nitroglycerine was not influenced by either active treatment. Conclusions: Raloxifene administration is associated with lower ICAM-1, VCAM-1 and Lp(a) plasma levels and enhanced endothelium dependent dilation compared to simvastatin although simvastatin is more powerful in total and LDL cholesterol reduction.     

Gender does not influence angiogenesis and arteriogenesis in a rabbit model of chronic hind limb ischemia

OBJECTIVE: Estrogen administration promotes angiogenesis and perfusion in oophorectomized rabbits with chronic limb ischemia. In the present study we tested whether gender affects angiogenesis and arteriogenesis in a rabbit model of chronic hind limb ischemia. METHODS AND RESULTS: Ischemia was induced in one hind limb of five oophorectomized (Ooph), seven non-oophorectomized (NonOoph) female and eight male New Zealand White rabbits by excision of the femoral artery. Ten days after the induction of ischemia (day 0) and at days 15 and 30 systolic calf blood pressure was measured in the ischemic and non-ischemic hind limbs. Revascularization in the ischemic limb was expressed as ischemic/normal limb blood pressure, capillary/muscle fiber density, and non-capillary, non-lymphatic vessels/muscle fiber density after examination of light microscopic sections taken from the abductor muscle of the ischemic limb at the time of death (day 30). Ischemic/normal blood pressure at day 30 in males was 0.62 +/- 0.22, in NonOoph 0.64 +/- 0.09 (P=ns vs. males) and in Ooph 0.39 +/- 0.05 (P<0.05 vs. males and NonOoph), (F=4.69, P=0.02). Ischemic capillary/muscle fiber in males was 0.96 +/- 0.09, in NonOoph 0.95 +/- 0.06 (P=ns vs. males) and in Ooph 0.83 +/- 0.09 (P<0.05 vs. males and NonOoph), (F=5.93, P=0.01). Ischemic non-capillary, non-lymphatic vessels/muscle fiber density in males was 0.11 +/- 0.02, in NonOoph 0.12 +/- 0.03 (P=ns vs. males) and in Ooph 0.08 +/- 0.02 (P<0.05 vs. NonOoph), (F=5.05, P=0.02). CONCLUSION: Gender does not influence angiogenesis and arteriogenesis in the rabbit model of chronic hind limb ischemia. However, estrogen deficiency induced by oophorectomy negatively affects angiogenesis and arteriogenesis.     

Monoclonal antibody detection of a circulating tumor-associated antigen. I. Presence of antigen in sera of patients with colorectal,gastric, and pancreatic carcinoma

Hybridoma-secreted monoclonal anti-colorectal carcinoma antibodies 19-9, 52a, and C₄ 14 bind specifically to cells of colorectal, gastric, and pancreatic carcinoma in tissue culture. The assay for the detection of antigen in human sera is based on the inhibition of binding of monoclonal antibodies to target preparations of colorectal carcinoma cells. Binding of monoclonal antibody 52a was inhibited more than 12% by 163 of 255 sera from patients from various stages of carcinoma of colon and rectum, by 45 of 49 sera from patients with pancreatic carcinoma, and by 8 of 11 sera from patients with gastric carcinoma. By contrast, only 7 of 89 sera from patients with other malignancies and 2 of 108 sera from healthy donors inhibited binding of this monoclonal antibody by more than 12%. These studies show the potential usefulness of monoclonal antibodies in the diagnosis of human malignancy.     

Expression of gC1q-R/p33 and its major ligands in human atherosclerotic lesions

A growing body of evidence supports the hypothesis that atherosclerosis has an inflammatory component, and that immune mechanisms, including complement activation, are likely to be involved. gC1q-R/p33 (gC1q-R) is a multifunctional and multicompartmental cellular protein, which is postulated to play a role in inflammation and thrombosis by interacting with C1q and high molecular weight kininogen (HK). To examine the expression of gC1q-R and its major ligands, C1q and HK, in human atherosclerotic lesions, sections of carotid arteries removed during endarterectomy and coronary arteries obtained at autopsy were stained with specific polyclonal or monoclonal antibodies. Control sections were stained with irrelevant rabbit IgG or isotype matched murine monoclonal antibody (MOPC), respectively. Tissue sections were counterstained with hematoxylin and examined by light microscopy. Specific staining for gC1q-R, C1q, and HK was observed in and around atherosclerotic lesions. In contrast to control antibodies, antibodies directed against gC1q-R reacted with endothelial cells, foam cells, smooth muscle cells, and inflammatory cells present in the intima and media of atherosclerotic lesions. In addition, the necrotic central core of advanced lesions with calcifications, fibrin, and lipids, stained intensely for gC1q-R, and negligibly with control antibodies. HK demonstrated a similar staining pattern, whereas C1q was most heavily expressed in the fibrous cap and necrotic core of atherosclerotic lesions. The localization of gC1q-R and its ligands C1q and HK in atherosclerotic lesions, and the previously described ability of gC1q-R to modulate complement, kinin, and coagulation cascades, suggest that gC1q-R may play an important role in promoting inflammation and thrombosis in atherosclerotic lesions.