Inhibition of adhesion molecules by budesonide on a human epithelial cell line (lung carcinoma)

Inhaled corticosteroids in the treatment of asthma have been shown to produce marked reductions in the number of inflammatory cells (mainly mast cells and eosinophils) and their products at bronchial level (such as cytokines). Recently, it has been demonstrated that epithelial cells express ICAM-1/CD54 in allergic patients both during natural allergen exposure and after allergen challenge. We have previously demonstrated that deflazacort (a systemic steroid) reduces the expression of ICAM-1 on conjunctival epithelial cells. The present study aimed to evaluate the effects exerted by budesonide on adhesion molecule expression by a human epithelial cell line (lung carcinoma: DM) and on soluble ICAM-1. Budesonide was added at concentrations corresponding to 10(-8), 10(-7), and 10(-6) mol/l in cultured epithelial cells, either in the absence of any stimulus or in the presence of interferon-gamma (IFN-gamma) at 500 U/ml. After 24 h of incubation, cytofluorometric analysis was performed for ICAM-1 and CD29/VLA beta 1. The 24-h supernatants of the same cultures were collected and then evaluated for soluble ICAM-1 (sICAM-1). The results showed that budesonide inhibits ICAM-1 and CD29 basal expression on the cells studied (P < 0.05): budesonide was effective in a dose-dependent manner. In addition, budesonide reduced surface ICAM-1 upregulation induced by IFN-gamma at 500 U/ml (P < 0.05). Finally, cell cultures with budesonide showed decreased levels of soluble ICAM-1 in basal condition, but not after IFN-gamma stimulation.     

Traumatic rupture of duodenal diverticulum. Report of a case and literature review

Duodenal diverticulum is a common anatomic abnormality. Its inflammatory perforation is a rare complication, with less than 100 cases reported in the available literature. Traumatic perforation is exceedingly rare (only 3 cases reported). In this report one more case of traumatic perforation is presented, and the literature is reviewed focusing on the pathogenic, diagnostic and therapeutic aspects of this severe disease.     

Involvement of ovarian steroids in the opioid-mediated reduction of insulin secretion in hyperinsulinemic patients with polycystic ovary syndrome

To evaluate the possible involvement of ovarian steroids on the opioid-mediated disorders of insulin in patients affected by polycystic ovary syndrome (PCOS), we studied 40 PCOS women. All patients underwent an oral glucose tolerance test (OGTT; 75 g) and basal hormone assay; based on the insulin response to OGTT, 26 women were classified as hyperinsulinemic and continued the study protocol. Patients were randomly divided into three groups characterized by different treatments: group A (nine patients) was treated with GnRH analog (one ampule every 28 days for 2 months), group B (eight patients) was treated with naltrexone (an oral opioid antagonist, 50 mg/day, orally) for 8 weeks, and group C (nine patients) was treated with GnRH analog plus naltrexone for 2 months. After continuation of treatment, all patients repeated the basal study in a second hospitalization. Naltrexone treatment significantly reduced the insulin response to OGTT, whereas GnRH analogue administration did not significantly change the insulin secretion after the glucose load. The GnRH analog/ naltrexone cotreatment was not able to influence the insulin secretory pattern; in fact, the insulin area under the curve was superimposable before and after therapy. These data could lead to the hypothesis that the opioidergic regulation of insulin secretion requires a normal steroidogenic pattern, thus suggesting that ovarian steroids modulate opioid activity also at peripheric districts.     

Effect of prosthesis type and size on the hemodynamic response of mitral valve prostheses to exertion

BACKGROUND: Doppler echocardiography is current tool for hemodynamic evaluation of mitral prosthetic heart valves. It's accepted that the area and the gradients by Doppler echocardiography are not influenced at rest by valvular type and valvular size. We evaluated the influence of valvular type, mechanical-biological, and size on exercise hemodynamic of normally-functioning mitral prosthesis. Thirty-seven patients with mitral prosthesis, mean age 56 +/- 10 years, underwent exercise Doppler echocardiography. Peak and mean prosthetic gradient were obtained at rest, during and at maximal exercise with a nonimaging transducer. Mechanical prosthesis were 23 and biological valves 14. Valvular size was less than 26 mm in 7 patients and more than 28 mm in 20 patients. Exercise increased the heart rate from 80 +/- 14 to 143 +/- 22 (p < 0.001), peak gradient from 11.4 +/- 4 to 26.1 +/- 7 mm Hg (p < 0.001) and mean gradient from 4.8 +/- 1 to 13.7 +/- 5 mm Hg (p < 0.001). We found similar peak (11.4 +/- 3 & 11.3 +/- 4) and mean gradient (3.4 +/- 1 & 2.9 +/- 0.7) at rest between mechanical and biological valves; at maximum exercise, peak (26 +/- 7 & 26 +/- 6) and mean gradient (13.9 +/- 6 & 13.2 +/- 4) were also similar. Prosthesis with > 28-mm-size compared with prosthesis < 26-mm-size showed minor peak gradient at second step (21.3 +/- 4 & 26.4 +/- 6, p < 0.05) and at peak exercise (25.4 +/- 7 & 29.8 +/- 8, ns). Hemodynamics on exercise using Doppler echocardiography was not influenced by valvular type (mechanical-biological) in normal mitral prosthesis. However, mitral prosthesis of small size showed worse on hemodynamics exercise than bigger ones.     

Histopathologic features in atherectomy samples obtained from patient with unstable angina, stable angina and restenosis. Directional Atherectomy Lombardi Group

BACKGROUND: The present study was aimed at investigating the pathologic features of directional coronary atherectomy (DCA) samples obtained from 194 patients (14 females) with stable (n = 68) and unstable (n = 95) angina, and with restenosis (n = 27). METHODS: DCA samples were obtained from culprit lesions, using the Simpson technique. Unstable angina was classified according to E. Braunwald criteria. Stable angina was grouped according to the presence or absence of a prior myocardial infarction (MI). DCA samples were fixed, processed, serially cut and stained with hematoxilin-eosin and with Movat pentachrome stain. RESULTS: The major pathologic findings were thrombosis, inflammation of the superficial plaque layers, and neointimal hyperplasia which often coexisted within a same sample. Their frequencies, in that order, were distributed in the differing groups of patients as follows: 21% (n = 9), 29.2% (n = 12) and 51% (n = 21) of the 41 cases with stable angina without prior MI. 40.7% (n = 11), 40.7% (n = 11), and 51.8% (n = 14) of the 27 cases with stable angina with prior MI. 25% (n = 4), 56.2% (n = 9) and 68.7% (n = 11), of the 16 cases with BI unstable angina. 35.3% (n = 14), 55.8% (n = 19) and 44% (n = 15), of the 34 cases with BII unstable angina. 44.4% (n = 4), 33.3% (n = 3) and 33.3% (n = 3), of the 9 cases with BIII unstable angina. 48.2% (n = 14), 48.2% (n = 14) and 51.8% (n = 15), of the 29 cases with CII unstable angina at 35.8 days after MI. 60% (n = 3), 60% (n = 3) and 40% (n = 2), of the 5 cases with CIII unstable angina at 8.3 days after MI. 26% (n = 7), 48% (n = 13) and 85.1% (n = 23), of the 27 cases with restenosis. According to above observation, the frequency of coronary thrombosis increases with the increase of the severity of myocardial ischemia. However, thrombosis is not found in most unstable angina without prior MI (63% of BI-II-III unstable angina cases do not have thrombus). In addition, thrombus is not a specific finding of unstable angina, given its occurrence, although in a much lower percentage of cases, in stable angina and in restenosis. CONCLUSIONS: Present data show that different ischemic and plaque lesions. This observation questions on the pathogenetic role of thrombus in unstable angina and calls for further investigations on inflammation and neointimal hyperplasia, as well as on the the reciprocal relation between these findings which are often combined within a same lesion.