Alexandros Nomikos

Immunohistochemical detection of E-cadherin in certain types of salivary gland tumours

OBJECTIVESnTo investigate the topography of E-cadherin and its possible correlation with the histological phenotype of salivary gland tumours.nnnMATERIAL AND METHODSnArchival formalin-fixed, paraffin-embedded sections of 54 benign and 56 malignant tumours and 24 samples of normal and inflamed salivary gland tissue were studied immunohistochemically using an Envision/horseraddish peroxidase (HRP) technique.nnnRESULTSnIn normal and inflamed salivary gland samples, E-cadherin was expressed at the membrane of acinar, myoepithelial and ductal cells located at cell-cell contact points. Reduction and/or absence of E-cadherin was only observed in pleomorphic adenoma at the peripheral cells of the duct-like or island structures, or in the cells exhibiting plasmacytoid or stromal differentiation. Neoplastic epithelium in Warthins tumours and in myoepithelial and oncocytic adenomas was strongly positive. Furthermore, a weak to moderate loss of expression which was related to tissue tumour subtype was seen in malignant tumours such as: adenoid cystic carcinomas; polymorphous low-grade adenocarcinomas; acinic cell carcinomas; and mucoepidermoid low-grade, epithelial-myoepithelial, lymphoepithelial and squamous low-grade carcinomas. Moderate to extreme loss or alternative cytoplasmic non-functional expression were observed in cases of salivary ductal carcinoma, carcinosarcoma, myoepithelial carcinoma, oncocytic adenocarcinoma, unspecified adenocarcinoma and squamous high-grade carcinomas.nnnCONCLUSIONnThis study suggests a direct association of E-cadherin expression with neoplastic histologic phenotype, which is lost in the more undifferentiated and invasive epithelial salivary gland tumours.

Statin treatment, carotid atherosclerotic plaque macrophage infiltration and circulating inflammatory markers.

Backround Statin treatment is considered as first line therapy in patients with atherosclerotic disease. We evaluated the effect of pre-treatment with statins on carotid plaque infiltration by macrophages and on the circulating levels of proinflammatory cytokines in patients who underwent carotid endarterectomy. Patients and Methods One hundred fourteen patients were enrolled; 89 men and 25 women (mean age 67±8 years; range 42-83 years). Fifty three patients (46%) were on statin treatment at least 3 months before endarterectomy and 61 (54%) had never received statin treatment. The serum levels of high sensitivity C reactive protein (hsCRP), serum amyloid A (SAA), tumor necrosis factor α (TNFα), interleukin (IL)-1β and IL-6 were evaluated preoperatively. The intensity of macrophage infiltration was evaluated by immunochemistry, using the monoclonal antibody CD 68. The area of the plaque covered by macrophages was measured as a proportion of the whole plaque area, using a custom designed image tool analysis. Results Patients on statins had lower serum total cholesterol levels (172±50 vs 194±35 mg/dl, p= 0.014), lower low density cholesterol levels (103±44 vs 123±31 mg/dl, p= 0.010) and lower serum hsCRP levels (1.8 [1.1-3.4] vs 3.4 [1.3-4.9] mg/l, p= 0.03), while SAA, TNFα, IL-6 and IL-1β levels did not differ between the 2 groups. The infiltration of atherosclerotic plaque by macrophages was similar in statin treated patients and in controls (0.55±0.15% vs 0.49±0.19%, p= 0.21). Conclusion Patients on statins have similar macrophage accumulation in their carotid atherosclerotic plaques compared with patients not on statins. Inflammatory markers were also similar in both groups except for hsCRP which was significantly lower in those taking statins.

Serum leptin levels in patients undergoing carotid endarterectomy: a pilot study.

Introduction: Elevated serum leptin levels are associated with cardiovascular events. We investigated the role of serum leptin in patients undergoing carotid endarterectomy (CEA). Methods: A total of 74 patients (55 men; 38 symptomatic and 36 asymptomatic; mean age 66.9 ± 8.2 years) undergoing CEA for >70% carotid artery stenosis were enrolled. Results: Serum leptin levels were lower in symptomatic compared with asymptomatic patients (7.1 ± 1.3 vs 14.4 ± 4.7 ng/dL; P < .001). Interleukin-6 (IL-6) levels were higher in symptomatic compared with asymptomatic patients (4.3 ± 1.7 vs 3.3 ± 1.1 pg/dL; P = .017). Symptomatic patients had more intense macrophage accumulation (0.7% ± 0.1% vs 0.3% ± 0.1%; P < .001). Serum leptin and serum IL-6 levels were independently associated with the presence of symptoms in multivariate analysis. Conclusion: Serum leptin levels were decreased in symptomatic carotid artery disease. This finding requires further investigation in larger studies.

The Effect of Negative Pressure Therapy on the Femoral Vein Blood Flow and Wall Structure

Negative pressure therapy has been recently used for managing lymphatic or infective groin complications. The aim of this study was to investigate any possible association between application of negative pressure therapy in the groin area and deep-vein thrombosis. Acute surgical wounds were created at the inguinal areas in 7 pigs. Different negative pressures ranging from −50 to −200 mmHg were applied directly over the femoral vessels, and blood flow alterations were studied using a Doppler ultrasound. Femoral vein specimens were also removed for histological examination after 12 hours of therapy. It has been demonstrated that negative pressure therapy does not significantly alter the baseline lower limb venous return. Histology demonstrated several changes, which are associated with vein thrombogenesis. The hemodynamic and pathological findings still leave a potential for thrombogenic effects of negative pressure therapy and warrant care to protect the femoral veins, with the use of thrombosis prophylaxis measures.