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Tip-enhanced Raman spectroscopy (TERS) is based on the optical excitation of localized surface plasmons in the tip-substrate cavity, which provides a large but local field enhancement near the tip apex. We report on TERS with smooth single crystalline surfaces as substrates. The adsorbates were CN- ions at Au(111) and malachite green isothiocyanate (MGITC) molecules at Au(111) and Pt(110) using either Au or Ir tips. The data analysis yields Raman enhancements of about 4 x 10(5) for CN- and up to 10(6) for MGITC at Au(111) with a Au tip, probing an area of less than 100 nm radius.

PTX3 is a prototypic long pentraxin expressed by various cell types, most prominently monocytes and endothelial cells, in response to interleukin-1 (IL-1), tumor necrosis factor (TNF) and bacterial products. In the present report, we show that interferon-gamma (IFN-gamma) inhibits the expression of the PTX3 gene induced by exposure to IL-1, TNF or lipopolysaccharide in human monocytes. This effect is dose dependent and observable when IFN-gamma is added from 24 h before up to 3 h after the addition of IL-1. While the time course of the IL-1-induced PTX3 mRNA expression is not affected, IFN-gamma reduces the stability of the PTX3 mRNA as well as its transcription. The inhibition of PTX3 expression is restricted to monocytes in that no inhibition occurs in cytokine-stimulated fibroblasts and endothelial cells. Under the same conditions, as expected, IFN-gamma augmented monocyte chemotactic protein-1 expression in the same cell preparations. PTX3 protein secretion by activated monocytes is also suppressed by exposure to IFN-gamma. Altogether, these data identify a negative pathway of regulation mediated by IFN-gamma, which may occur under inflammatory conditions.

Pentraxins, which include C reactive protein (CRP) and serum amyloid P component (SAP), are prototypic acute phase reactants that serve as indicators of inflammatory reactions. Here we report genomic and cDNA cloning of mouse ptx3 (mptx3), a member of the pentraxin gene family and characterize its extrahepatic expression in vitro and in vivo. mptx3 is organized into three exons on chromosome 3: the first (43 aa) and second exon (175 aa) code for the signal peptide and for a protein portion with no high similarity to known sequences the third (203 aa) for a domain related to classical pentraxins, which contains the "pentraxin family signature." Analysis of the N terminal portion predicts a predominantly alpha helical structure, while the pentraxin domain of ptx3 is accommodated comfortably in the tertiary structure fold of SAP. Normal and transformed fibroblasts, undifferentiated and differentiated myoblasts, normal endothelial cells, and mononuclear phagocytes express mptx3 mRNA and release the protein in vitro on exposure to interleukin-1beta (IL-1beta) and tumor necrosis factor (TNF)alpha. mptx3 was induced by bacterial lipopolysaccharide in vivo in a variety of organs and, most strongly, in the vascular endothelium of skeletal muscle and heart. Thus, mptx3 shows a distinct pattern of in vivo expression indicative of a significant role in cardiovascular and inflammatory pathology.

In this report we discuss the role of interferon regulatory factor 1 (IRF-1) in the regulation of ornithine decarboxylase (ODC) transcription during IFN gamma human macrophage activation. We show that a binding sequence for the transcription factor IRF-1 is contained in the first intron of the human ODC gene (from nt +2711 to nt +2722) and we demonstrate that the level of expression of IRF-1 increases in human macrophages and in the human promonocytic cell line, U937, previously differentiated in monocytes/macrophages by phorbol myristate acetate (PMA), after 2 h of IFN gamma stimulation. We also show that the hamster tk-ts13 cell line, stably transfected with the IRF-1 cDNA, over-expresses ODC. In addition, a specific complex was detected, by gel-shift assay after incubating a 20 bp double-stranded oligomer containing the binding sequence for IRF-1 with nuclear proteins extracted from human macrophages and from (PMA-differentiated) U937 cells stimulated with IFN gamma for 2 h.

In 5 patients with frequent premature ventricular ectopic beats, refractory to other antiarrhythmic treatments, amiodarone, given orally at the dose of 200 mg once a day for 4 weeks, reduced beta-adrenoceptor density from 202.9 +/- 62 to 101.1 +/- 33 fmol/mg protein (p < 0.01). Similarly, kd decreased from 21.0 +/- 6 to 3.9 +/- 1 (p < 0.05). Changes in beta-adrenoceptor population were accompanied by a marked reduction in mean premature ventricular complexes (PVC) frequency from the control value of 428.9 +/- 150.3 to 13.4 +/- 10.7 PVC/h (p < 0.05) and by a decrease in heart rate, from 83.8 +/- 4 to 73.9 +/- 4 b/min (p < 0.01). On the contrary, mean arterial pressure remained unchanged. Patients did not show side effects during treatment. Therefore, low dose oral amiodarone has important pharmacologic and therapeutic effects. It significantly reduces lymphocyte beta-adrenoceptor density and is effective in treatment of ventricular arrhythmias. Additional studies were performed in vitro exposing lymphocytes to increasing concentrations of amiodarone. The analysis of variance for repeated measures showed that amiodarone-induced reduction in lymphocyte beta-adrenoceptor density is a dose-depending phenomenon. Accordingly, treatment with doses of amiodarone higher than that used in the present study may induce a major reduction in lymphocyte beta-receptor density and exert a depressant cardiac effect.

In order to detect subclinical levels of Doxorubicin (D) cardiotoxicity, 21 patients aged 42 +/- 8 years with malignancies and treated with D as a part of a multiple regimen, were evaluated. The mean cumulative dose of D was 242 +/- 112 mg.m-2 (150 to 520 mg.m-2). Patients with systemic hypertension, valvular diseases, suspected coronary artery disease, ejection fraction less than 55% as assessed by radionuclide angiography, and aged more than 50 years were excluded from the study. A Doppler echocardiographic examination was performed before and after the course of D therapy with a mean interval of 142 days. The following variables were assessed: fractional shortening (FS), ejection fraction (EF), stroke volume (SV), isovolumic relaxation time (IVRT), maximal early diastolic flow velocity (Emax), maximal late diastolic flow velocity (Amax), and mitral deceleration time (Mdt). Indices derived from 19 aged-matched normal subjects were compared to those of the patients before the course of therapy. Doppler echocardiographic measurements did not differ significantly between the control group and patients before the course of therapy. While there were no significant changes in FS, EF, and SV in the study group before and after therapy, indices of diastolic filling showed striking differences: IVRT changed from 72 +/- 11 to 87 +/- 19 ms (P less than 0.001), Emax from 81 +/- 12 to 65 +/- 17 cm.s-1 (P less than 0.001), Mdt from 174 +/- 25 to 183 +/- 34 ms (P less than 0.05), Amax from 44 +/- 17 to 52 +/- 16 cm.s-1 (P less than 0.01). These data demonstrate impaired diastolic filling after doxorubicin therapy at conventional dosages.

In this paper a new computer aided ECG and VCG data handling is analized. It is based on an optimum estimation of dipole moment, which is used as the main diagnosis parameter. Already known diagnostical methods (available in present literature) are compared with this new technique. The available diagnostical range has been increased widely. The sensitivity of such a program is being analyzed both for normal and abnormal cases.