Search Results - (Author, Cooperation:G. Pesce)

2014-05-24

American Association for the Advancement of Science (AAAS)

0036-8075

1095-9203

Biology

Chemistry and Pharmacology

Computer Science

Medicine

Natural Sciences in General

Physics

1471-4159

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Abstract: Autoregulatory mechanisms affecting serotonin [5-hydroxytryptamine (5-HT)] release and synthesis during the early period of development were investigated in dissociated cell cultures raised from embryonic rostral rat rhombencephalon. The presence of 5-HT1A and 5-HT1B receptors in serotoninergic neurons was assessed using binding assays. The involvement of 5-HT1A and 5-HT1B receptors in the control of the synthesis and release of [3H]5-HT was studied using biochemical approaches with several serotoninergic receptor ligands. A mean decrease of 30% in [3H]5-HT synthesis and release was observed in the presence of 5-HT (10−8M), the 5-HT1A agonist 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT), the 5HT1B/1A agonist 5-methoxy-3-(1,2,5,6-tetrahydro-4-pyridinyl)-1H-indole (RU 24969), the 5-HT1B agonist 3-(1,2,5,6-tetrahydropyrid-4-yl)pyrrolo[3,2-b]pyrid-5-one (CP-93, 129), and the 5-HT1D/1B agonist sumatriptan. Inhibition of 5-HT synthesis and release induced by 8-OH-DPAT was blocked by chiral N-tert-butyl-3-[1-[1-(2-methoxy)phenyl]piperazinyl]-1-phenylpropionamide dihydrochloride quaternary-hydrate (WAY 100135) (10−7M) or methyl 4-[4-[4-(1,1,3-trioxo-2H-1,2-benzoisothiazol-2-yl)butyl]-1-piperazinyl]-1H-indole-2-carboxylate (SDZ 216–525) (10−7M), and that of CP-93, 129 was blocked by methiothepin (10−7M). Paradoxically, extracellular levels of [3H]5-HT increased in the presence of 8-OH-DPAT and RU 24969 at 10−6M. 5-HT uptake experiments showed that these two agonists interacted with the 5-HT transporter. 5-HT1 binding sites (620 fmol/mg of protein) and 5-HT1A (482 fmol/mg of protein) and 5-HT1B (127 fmol/mg of protein) receptors were detected in 12-day in vitro cell cultures. Experiments carried out with tetrodotoxin suggested that 5-HT1A receptors are located on nerve cell bodies, whereas 5-HT1B receptors are located on the nerve terminals. We concluded that autoregulatory mechanisms involving 5-HT1A and 5-HT1B autoreceptors are functionally mature in cells from rostral raphe nuclei during the early period of development.

Electronic Resource

1398-9995

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

The protective effects of deflazacort against the inflammation that follows the conjunctival provocation test (CPT) by specific allergen were assessed in 24 patients with rhinoconjunctivitis caused by Parietaria judaica in a double-blind study. After a screening CPT, patients were randomized into four treatment groups, each being given deflazacort (oral tablets) at 6, 30, and 60 mg once daily, or matching placebo, for 3 d, outside the pollen season. Clinical evaluation (itching, hyperemia, lacrimation, and swelling of eyelids) and cytologic assessment (number of inflammatory cells in conjunctival scraping and evaluation of ICAM (intercellular adhesion molecule)-1/CD54 expression on epithelial cells) were performed at base line, 30 min (early-phase reaction (EPR), 6 h and 24 h (late-phase reaction (LPR)) after specific CPT, and before and after treatment. Neither the EPR clinical reactions nor the EPR total number of inflammatory cells was modified by deflazacort. However, the LPR clinical effects were significantly reduced by deflazacort at 30 or 60mg/d (P〈0.01), as compared with placebo. The total number of inflammatory cells during LPR was significantly reduced by deflazacort at 30 or 60 nig/d ((P〈0.01), as compared with placebo. Furthermore, CD54 expression was significantly reduced by deflazacort at 30 or 60 mg/d both in the EPR ((P〈0.01) and LPR ((P〈0.01), as compared with placebo. None of the studied indicators were modified at the 6 mg/d dose. This study shows that deflazacort has a highly protective action against clinical and cellular LPR effects induced by the specific CPT, In addition, deflazacort markedly reduces CD54 expression on the conjunctival epithelium during both EPR and LPR.

Electronic Resource

1365-2222

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Background The intercellular adhesion molecule ICAM-1 has been detected by immunohistochemical methods on epithelial cells of the conjunctiva and nose during allergic inflammation.Objective The aim of the present study was to evaluate whether ICAM-1 expression on conjunctival epithelium derives from endogenous synthesis or is merely due to passive uptake of soluble ICAM-1 released from inflammatory cells.Methods In situ hybridization was performed using a 3’end dygoxygenin-labelled specific DNA oligonucleotide probe on fixed conjunctival smears from allergic subjects challenged with, or naturally exposed to the allergen, and from healthy subjects. Immunocytochemistry for ICAM-1 was performed by alkaline phosphatase antialkaline phosphatase.Results Results In allergic patients, both naturally exposed to the allergen and after specific challenge, a clear hybridization pattern on epithelial cells was apparent. Out of allergen exposure, some symptomfree pollinosic subjects, as well as a few healthy volunteers showed mild ICAM-1 mRNA cytoplasmic staining in the absence of immunohistochemically detectable ICAM-1. This finding may explain the very early appearance of ICAM-1 on conjunctival epithelium following specific challenge in allergic individuals.Conclusions These results indicate that the presence of ICAM-1 on conjunctival epithelium during allergic inflammation derives from endogenous synthesis and not from uptake of soluble ICAM-l.

Electronic Resource

1365-2222

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Background Azelastine is a selective H1-receptor antagonist, which has previously been demonstrated to be effective in the treatment of allergic rhinitis. We have recently demonstrated that nasal azelastine inhibits the clinical and intlammatory events following nasal allergen challenge. Particularly, we focused our attention on ICAM-1 expression on epithelial cells, since it is the natural ligand of LFA-1, an adhesion molecule expressed by leucocytes, including eosinophils.Objective Since azelastine ocular drops are now available, the aim of the present study was the evaluation of the anti-allergic activity in the model of allergen specific conjunctival challenge (ASCC).Methods Twenty outpatients with allergic rhinoconjunctivitis due to Parietaria Judaica (Wall Parietary) were included outside the pollen season. The study was designed as randomized, placebo-controlled, double-blind and parallel group, developed in two parts. The fonner investigated the onset of effect of a single dose of azelastine eye drops administered 20min after clinical response due to ASCC. The latter evaluated the clinical and inflammatory parameters following ASCC after 7-days treatment with azelastine. Clinical parameters (hyperaemia, itching, lacrimation and eyelid swelling) were evaluated at baseline, 5, 10, 20 and 30 min (i.e. early phase reaction-EPR) and 6h (i.e. late phase reaction-LPR) after ASCC. Cytological assessment (number of neutrophils, eosinophils. monocytes and lymphocytes) and ICAM-1 expression on conjunctival epithelial cells were evaluated at baseline, 30 min (i.e. early phase reaction-EPR) and 6h (i.e. late phase reaction-LPR) after ASCC.Results When administered 30 min after ASCC, azetastine produced a clinical effect ranging between 10 and 20 min after eye drops administration (P 〈 0.01). After 7 days of treatment, 30 min after ASCC, azelastine induced a reduction of symptom scores during EPR and LPR (P〈0.01), a reduction of inflammatory cell infiltration during both EPR (P 0.01) and LPR (P 0.01), and a reduction of ICAM-1 expression during EPR and LPR (both P 0.01). Placebo did not modify any of the studied parameters.Conclusion Azelastine eye drops exert anti-allergic activity, inducing a rapid improvement of clinical events when administered after ASCC, and reducing both sytiiptoms and cellular infiltration when administered before ASCC. Finally, azelastine down-regulates ICAM-1 expression on epithelial conjunctival cells, confirming the results obtained at nasal level.

Electronic Resource

1365-2222

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Background Levocabastine is a selective topical H1 antagonist, effective in the treatment of seasonal allergic rhinitis and conjunctivitis.Objective We evaluated the possible effects of levocabastine eye drops on early (EPR) and late phase (LPR) inflammatory changes induced by allergen-specific conjunctival challenge (ASCC). We focused our attention on the possible effect of levocubastine on expression of the intracellular adhesion molecule-1 (ICAM-1) on epithelial cells. Such a phenomenon is likely to play an important role in allergic inflammation.Methods The study was a double-blind, placebo-controlled, randomized trial, performed in cross-over, outside the pollen season. Ten out-patients suffcring from allergic rhinoconjunctivitis due to Parietaria Judaica (wall parietary) were enrolled. Patients randomly received levocabastine eye drops (0.5 mg/mL) or placebo eyedrops, one drop in the left eye (right eye as control), 30 min before ASCC. Clinical evaluation (hyperaemia, burning-itching, lacrimation and eyelid swelling) and cytological assessment (number of neutrophils, eosinophils and lymphocytes, and ICAM-1 expression on conjunctival epithelium) were evaluated at baseline, 30min and 6h after ASCC. In parallel, we evaluated the in vitro effect of levocabastine at concentrations ranging from 2 × 10−9 M to 2 × 10−5M on ICAM-l expression and shedding by a continuously cultured differentiated epithelial cell line (WK).Results Levocabastine reduced symptom scores during EPR (15min and 30min, P 〈 0.002), inflammatory cell infiltration duritig FPR (P 〈 0.002 for neutrophils, eosinophils and lymphocytes) and ICAM-1 expression on epithelium both during EPR (P 〈 0.002) and LPR (P 〈 0.02). LPR symptom scores and inflammatory cell infiltration were only slightly modified by levocabastine treatment. In vitro levocabastine at 2 ± 10−5 M concentration was able to down-regulate basal ICAM-1 expression, although it exerted no effect on ICAM-1 expression by interferon-γ (IFNγ)-stimulated WK cells and on soluble ICAM-1 release by epithelium.Conclusion Levocabastine exerts anti-allcrgJc activity, in that it reduces in vivo inflammatory cell infiltration due to ASCC, and also adhesion molecule expression on conjunctival epithelium. The latter phenomenon may be due, at least in part, to a direct effect of levocabastine on epithelial cells.

Electronic Resource

1398-9995

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Canonica GW, Ciprandi G, Buscaglia S, Pesce G, Bagnasco M. Adhesion molecules of allergic inflammation: recent insights into their functional roles.

Electronic Resource

1398-9995

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Paolieri F, Battifora M, Riccio AM, Pesce G, Canonica GW, Bagnasco M. Intercellular adhesion molecule-1 on cultured human epithelial cell lines: influence of proinflammatory cytokines.The expression of intercellular adhesion molecule-1 ‘CD54 or ICAM-1’ on epithelial cells during acute or chronic inflammation may favor the interaction between epithelial cells and leukocytes expressing the natural ligands of ICAM-1, LFA-1 ‘CD11a/CD18’, and Mac-1 ‘CD11b/CD18’. We have evaluated in vitro the expression of ICAM-1 by a conjunctival ‘WK’ and an intestinal ‘1407’ human continuous epithelial cell line. Cells were cultured for 24 h in the presence or absence of IFN-γ, TNF-α, IL-1β, IL-4, IL-6, IL-8, IL-10, and TGF-Jβ1. Both epithelial cell lines showed a constitutive expression of ICAM-1. IFN-γ at 500 U/ml and TNF-α at 200 ng/ml upregulated ICAM-1 expression; IL-1β at 100 pg/ml upregulated ICAM-1 on WK cells only. Cells cultured in the presence of both IFN-γ and TNF-α exhibited a mean fluorescence intensity far greater than those cultured with IFN-γ or TNF-α alone. 1407 and WK cells were able to release soluble ICAM-1. IFN-γ and TNF-α enhanced the release of sICAM-1. IL-4, IL-6, IL-8, IL-10, and TGF-β1 did not affect either ICAM-1 expression or sICAM-1 release. In conclusion, continuously cultured human epithelial cells may express ICAM-1 on their surface and release it in culture medium. These phenomena are upregulated by proinflammatory cytokines.

Electronic Resource

1398-9995

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Background: Tissue transglutaminase (t-TG) is the main autoantigen recognized by the endomysium antibodies (EMA) observed in patients with celiac disease (CD). The aim of the study was to assess an ELISA method for t-TG antibodies (t-TGA) with respect to EMA IF assay in pediatric and adult patients. Methods: t-TGA were analyzed by ELISA in 220 sera samples: 82 patients with biopsy-proven untreated CD (23 adults and 59 children), 14 CD children on gluten-free diet, 18 asymptomatic relatives of CD patients, and 106 age-matched control patients with gluten-unrelated gastrointestinal diseases (58 adults and 48 children). Serum IgA EMA were tested on umbilical cord sections in all patients. Results: The great majority (92.7%) of untreated CD patients (both adults and children) were t-TGA positive (values ranging from 20.1 to 〉300 AU). None of the child control patients and only two out of 58 (3.4%) of the adults with unrelated gastrointestinal diseases had serum t-TGA positivity; two out of 18 first-degree relatives with biopsy-proved silent CD were t-TGA (as well as EMA) positive. Finally, two out of 14 CD children, assuming a gluten-free diet, had serum t-TGA (as well as EMA). A highly significant correlation (P〈0.001) was observed between t-TGA concentrations and EMA. t-TGA showed a sensitivity of 87% and 95%, a specificity of 97% and 100% for adults and children, respectively. Conclusions: The method is highly sensitive and specific in the diagnosis of CD and is promising as a tool for routine diagnostic use and population screening, especially in children.

Electronic Resource

1365-2133

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Electronic Resource

0040-4020

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Chemistry and Pharmacology

Electronic Resource

0022-328X

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Chemistry and Pharmacology

Electronic Resource

0022-328X

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Chemistry and Pharmacology

Electronic Resource

0196-9781

Endocrine pancreas ; Mechanisms of pancreatic TRH secretion ; Perinatal period ; TRH

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Chemistry and Pharmacology

Electronic Resource

1398-9995

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

Electronic Resource

1398-9995

Blackwell Publishing Journal Backfiles 1879-2005

Medicine

We performed the serum IgA antiendomysium antibody (EmA) assay by indirect immunofluorescence on human umbilical cord sections in 86 subjects with celiac disease, in 187 first-degree relatives of such patients, and in a control group of 68 unrelated subjects, to investigate the suitability of the method in the screening of populations at risk of gluten sensitivity. Conventional EmA assay using monkey esophagus sections was performed in parallel experiments. The results obtained showed a perfpect correlation between the two methods. All the celiac patients and none of the controls were positive for EmA. EmA positivity was also observed in 11 apparently healthy relatives: intestinal biopsy performed in five of them invariably showed villous atrophy and increase of mucosal lymphocytes. Taking into account the low cost of EmA assay on human umbilical cord, especially when compared to monkey esophagus sections, the method is probably suitable and effective in identifying latent, asymptomatic gluten sensitivity in at-risk populations.

Electronic Resource

1530-0358

Rectum ; Hemorrhage ; Ulcerative colitis ; Adrenaline chloride ; Washout ; Surgical technique

Springer Online Journal Archives 1860-2000

Medicine

Abstract Three patients suffering from ulcerative colitis, who had previously undergone a colectomy and temporary Brooke ileostomy and who were under treatment with methylprednisolone and 5-aminosalicylic acid per the rectum, were readmitted to the hospital, presenting with profuse rectal hemorrhage with six to nine blood losses per day. An adrenaline chloride solution washout of the rectum was given in an attempt to avoid surgery. In the two to six hours after treatment, hemorrhage was considerably reduced, the hemoglobin levels were stationary, and no further transfusions were necessary.

Electronic Resource

1432-0649

PACS: 07.65; 33; 42.68

Springer Online Journal Archives 1860-2000

Physics

Abstract.  An AlGaAs diode laser was used to detect NO2 absorption lines belonging to the (0 0 0)–(2 13 1) vibrational band, within the X˜2 A 1 electronic ground state, at 739 nm. A simple absorption spectrometer based on wavelength-modulation spectroscopy with second-harmonic detection was developed. The minimum detectable pressure of pure NO2 was 0.1 μbar with 2 m absorption path-length, corresponding to an absorbance of 10-6. High-sensitivity detection of NO2 was also performed in the presence of N2 and air at different total pressures: The effects on the detection limit of our apparatus were accurately investigated. The minimum NO2 concentration at 500 mbar of air was measured to be 2 ppm.

Electronic Resource

0040-4039

Elsevier Journal Backfiles on ScienceDirect 1907 - 2002

Chemistry and Pharmacology

Electronic Resource

1432-1041

CD54 (intercellular adhesion molecule-1 [ICAM-1]) ; Conjunctival provocation test ; Deflazacort ; early phase reaction ; inflammatory response ; late phase reaction

Springer Online Journal Archives 1860-2000

Chemistry and Pharmacology

Medicine

Summary The protective effects of deflazacort, (a new heterocyclic glucocorticoid and derivative of prednisolone, with calcium and glucose-sparing effects) on the inflammatory reaction following an allergen-specific conjunctival provocation test (CPT) were assessed in a doubleblind study, in 24 patients suffering from rhinoconjunctivitis due toParietaria judaica. After an initial screening CPT, patients were randomized to four treatment groups, to receive deflazacort, 6, 30 or 60 mg, once daily or placebo, for 3 days, during the low-pollen season. Clinical evaluations (itching, hyperaemia, lacrimation and eyelid swelling), cytological assessment (number of inflammatory cells, i. e. neutrophils, eosinophils and lymphocytes, sampled by conjunctival scraping) and immunocytochemical evaluation of CD54 (intercellular adhesion molecule-1 [ICAM-1]) expression on epithelial cells were performed after CPT, at baseline, after 30 minutes (early-phase reaction [EPR]) and after 6 and 24 hours (late-phase reaction [LPR]), before and after treatment. Neither the nature or severity of clinical events nor the total number of inflammatory cells during the EPR changed during treatment with deflazacort. The severity of the clinical events during the LPR were significantly reduced by deflazacort, 30 and 60 mg/dayP 〈 0.01) compared to the placebo-treated group. The total number of inflammatory cells during the LPR was also significantly reduced by deflazacort, 30 and 60 mg/ day (P 〈 0.01) compared to the placebo-treated group. CD54 expression was significantly reduced by deflazacort, 30 and 60 mg/day both during the EPR (P 〈 0.01) and LPR (P 〈 0.01) compared to the placebo-treated group. Deflazacort, 6 mg/day did not significantly alter clinical, cellular or immunocytochemical variables compared to the placebo-treated group. This study shows that deflazacort has a highly protective effect on clinical and cellular LPR events induced by specific CPT. In addition, deflazacort markedly reduces CD54 expression on conjunctival epithelium during both the EPR and LPR.

Electronic Resource