Annals of the New York Academy of SciencesVolume 886, Issue 1 p. 212-216 Truncated Form of β-Catenin and Reduced Expression of Wild-Type Catenins Feature HepG2 Human Liver Cancer Cells GIUSEPPE CARRUBA, Corresponding Author GIUSEPPE CARRUBA Institute of Oncology, University of Palermo, Palermo, Italy Address for correspondence: Institute of Oncology, Via Marchese Ugo 56, 90141 Palermo, Italy. Phone +39 091 666-4346; fax, +39 091 666–4352. e-mail, [email protected]Search for more papers by this authorMELCHIORRE CERVELLO, MELCHIORRE CERVELLO Institute of Developmental Biology, C.N.R., Palermo, ItalySearch for more papers by this authorMARIA D. MICELI, MARIA D. MICELI Institute of Oncology, University of Palermo, Palermo, ItalySearch for more papers by this authorROSARIA FARRUGGIO, ROSARIA FARRUGGIO Institute of Oncology, University of Palermo, Palermo, ItalySearch for more papers by this authorMONICA NOTARBARTOLO, MONICA NOTARBARTOLO Experimental Oncology, Palermo Branch of IST-Genoa, c/o M. Ascoli Cancer Hospital Center, Palermo, ItalySearch for more papers by this authorLUCREZIA VIRRUSO, LUCREZIA VIRRUSO Institute of Developmental Biology, C.N.R., Palermo, ItalySearch for more papers by this authorLYDIA GIANNITRAPANI, LYDIA GIANNITRAPANI Institute of Internal Medicine, University of Palermo, Palermo, ItalySearch for more papers by this authorROBERTO GAMBINO, ROBERTO GAMBINO Institute of Developmental Biology, C.N.R., Palermo, ItalySearch for more papers by this authorGIUSEPPE MONTALTO, GIUSEPPE MONTALTO Institute of Internal Medicine, University of Palermo, Palermo, ItalySearch for more papers by this authorLUIGI CASTAGNETTA, LUIGI CASTAGNETTA Institute of Oncology, University of Palermo, Palermo, Italy Experimental Oncology, Palermo Branch of IST-Genoa, c/o M. Ascoli Cancer Hospital Center, Palermo, ItalySearch for more papers by this author GIUSEPPE CARRUBA, Corresponding Author GIUSEPPE CARRUBA Institute of Oncology, University of Palermo, Palermo, Italy Address for correspondence: Institute of Oncology, Via Marchese Ugo 56, 90141 Palermo, Italy. Phone +39 091 666-4346; fax, +39 091 666–4352. e-mail, [email protected]Search for more papers by this authorMELCHIORRE CERVELLO, MELCHIORRE CERVELLO Institute of Developmental Biology, C.N.R., Palermo, ItalySearch for more papers by this authorMARIA D. MICELI, MARIA D. MICELI Institute of Oncology, University of Palermo, Palermo, ItalySearch for more papers by this authorROSARIA FARRUGGIO, ROSARIA FARRUGGIO Institute of Oncology, University of Palermo, Palermo, ItalySearch for more papers by this authorMONICA NOTARBARTOLO, MONICA NOTARBARTOLO Experimental Oncology, Palermo Branch of IST-Genoa, c/o M. Ascoli Cancer Hospital Center, Palermo, ItalySearch for more papers by this authorLUCREZIA VIRRUSO, LUCREZIA VIRRUSO Institute of Developmental Biology, C.N.R., Palermo, ItalySearch for more papers by this authorLYDIA GIANNITRAPANI, LYDIA GIANNITRAPANI Institute of Internal Medicine, University of Palermo, Palermo, ItalySearch for more papers by this authorROBERTO GAMBINO, ROBERTO GAMBINO Institute of Developmental Biology, C.N.R., Palermo, ItalySearch for more papers by this authorGIUSEPPE MONTALTO, GIUSEPPE MONTALTO Institute of Internal Medicine, University of Palermo, Palermo, ItalySearch for more papers by this authorLUIGI CASTAGNETTA, LUIGI CASTAGNETTA Institute of Oncology, University of Palermo, Palermo, Italy Experimental Oncology, Palermo Branch of IST-Genoa, c/o M. Ascoli Cancer Hospital Center, Palermo, ItalySearch for more papers by this author First published: 06 February 2006 https://doi.org/10.1111/j.1749-6632.1999.tb09419.xCitations: 38Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onEmailFacebookTwitterLinkedInRedditWechat REFERENCES 1 Takeichi, M. 1991. Cadherin cell adhesion receptor as a morphogenetic regulator. Science (Washington, DC) 251: 1451–1455. 2 Kemler, R. 1993. From cadherins to catenins: Cytoplasmic protein interactions and regulation of cell adhesion. Trends Genet. 9: 317–321. 3 Shimoyama, Y., A. Nagafuchi, S. Fujita, M. Gotoh, M. Takeichi, S. Tsukita & S. Hirohashi. 1992. Cadherin dysfunction in a human cancer cell line: Possible involvement of loss of α-catenin expression in reduced cell-cell adhesiveness. Cancer Res. 52: 5770–5774. 4 Nakanishi, Y., A. Ochiai, S. Akimoto, H. Kato, H. Watanabe, Y. Tachimori, S. Yamamoto & S. Hirohashi. 1997. Expression of E-cadherin, α-catenin, β-catenin and plakoglobin in esophageal carcinomas and its prognostic significance. Oncology 54: 158–165. 5 Laemmli, U.K. 1970. Cleavage of structural proteins during the assembly of the head of bacteriophage T4. Nature 227: 680–685. 6 Chomczynski, P. & N. Sacchi. 1987. Single-step method of RNA isolation by acidic guanidinium thiocyanate-phenol-chloroform extraction. Anal. Biochem. 162: 156–159. 7 Yost, C., M. Torres, J.R. Miller, E. Huang, D. Kimelman & R.T. Moon. 1996. The axis-inducing activity, stability and subcellular distribution of β-catenin is regulated in Xenopus embryo by glycogen synthase kinase 3. Genes Dev. 10: 1443–1454. 8 DeLa Coste, A., B. Romagnolo, P. Billuart, C.A. Renard, M.-A. Buendia, O. Soubrane, M. Fabre, J. Chelly, C. Beldiord, A. Kahn & C. Perret. 1998. Somatic mutations of the β-catenin gene are frequent in mouse and human hepatocellular carcinoma. Proc. Natl. Acad. Sci. USA 95: 8847–8851. Citing Literature Volume886, Issue1ANTICANCER MOLECULES: STRUCTURE, FUNCTION, AND DESIGNDecember 1999Pages 212-216 ReferencesRelatedInformation

Annals of the New York Academy of SciencesVolume 876, Issue 1 p. 426-429 Sex Hormones Modulate Inflammatory Mediators Produced by Macrophagesa P. D'AGOSTINO, P. D'AGOSTINO Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalySearch for more papers by this authorS. MILANO, S. MILANO Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalySearch for more papers by this authorC. BARBERA, C. BARBERA Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalySearch for more papers by this authorG. DI BELLA, G. DI BELLA Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalySearch for more papers by this authorM. LA ROSA, M. LA ROSA Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalySearch for more papers by this authorV. FERLAZZO, V. FERLAZZO Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalySearch for more papers by this authorR. FARRUGGIO, R. FARRUGGIO Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, Italy Institute of Oncology, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalySearch for more papers by this authorD. M. MICELI, D. M. MICELI Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, Italy Institute of Oncology, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalySearch for more papers by this authorM. MIELE, M. MIELE Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, Italy Institute of Oncology, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalySearch for more papers by this authorL. CASTAGNETTA, L. CASTAGNETTA Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, Italy Institute of Oncology, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalySearch for more papers by this authorE. CILLARI, Corresponding Author E. CILLARI Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalyAddress correspondence to Prof. Enrico Cillari, Institute of General Pathology, Corso Tukory 211, 90134 Palermo, Italy. Tel: 091-6555913; fax: 091-6555901.Search for more papers by this author P. D'AGOSTINO, P. D'AGOSTINO Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalySearch for more papers by this authorS. MILANO, S. MILANO Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalySearch for more papers by this authorC. BARBERA, C. BARBERA Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalySearch for more papers by this authorG. DI BELLA, G. DI BELLA Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalySearch for more papers by this authorM. LA ROSA, M. LA ROSA Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalySearch for more papers by this authorV. FERLAZZO, V. FERLAZZO Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalySearch for more papers by this authorR. FARRUGGIO, R. FARRUGGIO Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, Italy Institute of Oncology, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalySearch for more papers by this authorD. M. MICELI, D. M. MICELI Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, Italy Institute of Oncology, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalySearch for more papers by this authorM. MIELE, M. MIELE Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, Italy Institute of Oncology, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalySearch for more papers by this authorL. CASTAGNETTA, L. CASTAGNETTA Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, Italy Institute of Oncology, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalySearch for more papers by this authorE. CILLARI, Corresponding Author E. CILLARI Institute of General Pathology, University of Palermo, Experimental Oncology Units, c/o M. Ascoli Hospital Center, University of Palermo, ItalyAddress correspondence to Prof. Enrico Cillari, Institute of General Pathology, Corso Tukory 211, 90134 Palermo, Italy. Tel: 091-6555913; fax: 091-6555901.Search for more papers by this author First published: 06 February 2006 https://doi.org/10.1111/j.1749-6632.1999.tb07667.xCitations: 156 a This work was supported by Assessorato dei Beni Culturali ed Ambientali della Pubblica Istruzione Regione Sicilia, 1996. Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat Citing Literature Volume876, Issue1NEUROENDOCRINE IMMUNE BASIS OF THE RHEUMATIC DISEASESJune 1999Pages 426-429 RelatedInformation

We investigated conversion rates of androgens to estrogens in cultured, hormone-responsive prostate (LNCaP) and breast (MCF-7) human cancer cells. For this purpose, we adopted an intact cell analysis, whereby cells were incubated for different incubation times in the presence of close-to-physiological (1 nM) or supraphysiological (1 microM) concentrations of labelled androgen precursors, i.e. testosterone (T) and androstenedione (delta4Ad). The aromatase activity, as measured by estrogen formation, was detected in LNCaP cells (0.5 pmol/ml), even though to a significantly lower extent than in MCF-7 cells (5.4 pmol/ml), using 1 microM T after 72 h incubation. Surprisingly, LNCaP cells displayed a much higher aromatase activity when T was used as a substrate with respect to delta4Ad. In either cell line, T transformation to delta4Ad was relatively low, attaining only 2.8% in LNCaP and 7.5% MCF-7 cells. However, T was mostly converted to conjugates (over 95%), glucuronides and some sulphates, in LNCaP cells, whereas it was only partly converted to sulphates (<10%) in MCF-7 cells. Aromatase activity seems to be inconsistent in LNCaP cells, being strongly affected by culture conditions, especially by fetal calf serum (FCS). Further studies should assess the regulation of aromatase expression by serum or growth factors in different human cancer cells, also using anti-aromatase and/or anti-estrogen compounds, in different culture conditions.

In the present study we have inspected estrogen metabolism in cultured human prostate cancer cells (LNCaP, DU145, PC3), in relation to the expression of mRNAs for different 17βhydroxysteroid dehydrogenase (17βHSD) enzymes (from 1 to 4). Using an intact cell analysis, we have compared precursor degradation and product formation after incubation of cells with physiological amounts of radioactive E2 or estrone (E1) for 24–72 h and subsequent reverse-phase high performance liquid chromatography analysis. The LNCaP and DU145 cells only partly converted E2 to E1 (26 and 13% at 72 h, respectively), giving rise to an appreciable production of E2 from E1 (nearly 20% in all cases). Conversely, PC3 cells revealed a massive E2 oxidation to E1 (up to 90% by 72 h) and a scant formation of E2 (<2%) from E1. In addition, an appreciable formation of 16αOHE1 was seen in either PC3 (11%) or DU145 (5%) cells, respectively using E2 or E1 as precursor. All three cell lines exhibited marked amounts of 17βHSD4 mRNA species, whilst even greater amounts of 17βHSD2 transcript were found in PC3 cells only. No mRNA for either 17βHSD1 or 17βHSD3 could be detected in any cell line. The present evidence indicates that pathways of estrogen metabolism are distinctly governed in prostate cancer cells depending on their endocrine status, being associated with a differential expression of mRNA for different 17βHSD enzymes.

Sex hormones have been proposed to play an important role in promoting liver cancer transformation. The aim of our study was to evaluate changes in circulating levels of estradiol (EII), testosterone (T) and the EII/T relationship (ETR) in patients with liver cirrhosis (LC) and hepatocellular carcinoma (HCC) of viral origin compared with a group of healthy controls (C). The study population included 64 patients (41 M) mean age 62.5 years with HCC; 68 patients (41 M) mean age 61.3 years suffering from LC, while the C included 59 subjects (39 M) mean age 60.0 years recruited from voluntary blood donors. EII and T were assayed using the IEMA method; ultrasonography was performed using a Toshiba SSA 240 A scanner with a convex 3.75 MHz probe. Serum EII levels progressively increased from C to LC and HCC with statistically significant values (H=36.9, p<0.0001). Serum values of T progressively decreased from C to LC and HCC but the difference was not significant (H=3.84, p=ns). ETR values differed in the three groups, with a significant difference between C vs LC and HCC (p<0.0001). There was also a significant difference for EII, with values decreasing as the neoplasm dimension increased (p<0.04), and in particular there were differences between HCC <5 cm vs >5 cm (p<0.05). In contrast, ETR progressively increased as the diameter of neoplasm increased, but differences were significant only between <3 cm vs >5 cm (p<0.05). In conclusion, our data confirm that in LC and HCC there is an increase in serum EII levels, which can be important in the genesis of liver carcinoma. Progressive serum reduction in T may be due to increased androgen uptake and progressive accumulation within the neoplastic mass. Further studies are necessary to determine whether subjects with LC and elevated serum levels of estrogens are at higher risk of developing HCC.

Annals of the New York Academy of SciencesVolume 784, Issue 1 p. 70-84 Multiple Estrogen Function in Human Prostate Cancer Cellsa GIUSEPPE CARRUBA, GIUSEPPE CARRUBA Hormone Biochemistry Laboratories School of Medicine University of Palermo Palermo, ItalySearch for more papers by this authorMARIA D. MICELI, MARIA D. MICELI Hormone Biochemistry Laboratories School of Medicine University of Palermo Palermo, ItalySearch for more papers by this authorLOREDANA COMITO, LOREDANA COMITO Experimental Oncology and Molecular Endocrinology Units Palermo Branch of the National Cancer Institute of Genoa “M. Ascoli”. Cancer Hospital Center Palermo, ItalySearch for more papers by this authorROSARIA FARRUGGIO, ROSARIA FARRUGGIO Hormone Biochemistry Laboratories School of Medicine University of Palermo Palermo, ItalySearch for more papers by this authorCARMELA M. G. SORCI, CARMELA M. G. SORCI Hormone Biochemistry Laboratories School of Medicine University of Palermo Palermo, ItalySearch for more papers by this authorGIUSEPPA OLIVERI, GIUSEPPA OLIVERI Hormone Biochemistry Laboratories School of Medicine University of Palermo Palermo, ItalySearch for more papers by this authorROSALBA AMODIO, ROSALBA AMODIO Hormone Biochemistry Laboratories School of Medicine University of Palermo Palermo, ItalySearch for more papers by this authorMARCO DI FALCO, MARCO DI FALCO Hormone Biochemistry Laboratories School of Medicine University of Palermo Palermo, ItalySearch for more papers by this authorDOMENICO D'AMICO, DOMENICO D'AMICO Hormone Biochemistry Laboratories School of Medicine University of Palermo Palermo, ItalySearch for more papers by this authorLUIGI A. M. CASTAGNETTA, LUIGI A. M. CASTAGNETTA Hormone Biochemistry Laboratories School of Medicine University of Palermo Palermo, Italy Experimental Oncology and Molecular Endocrinology Units Palermo Branch of the National Cancer Institute of Genoa “M. Ascoli”. Cancer Hospital Center Palermo, ItalySearch for more papers by this author GIUSEPPE CARRUBA, GIUSEPPE CARRUBA Hormone Biochemistry Laboratories School of Medicine University of Palermo Palermo, ItalySearch for more papers by this authorMARIA D. MICELI, MARIA D. MICELI Hormone Biochemistry Laboratories School of Medicine University of Palermo Palermo, ItalySearch for more papers by this authorLOREDANA COMITO, LOREDANA COMITO Experimental Oncology and Molecular Endocrinology Units Palermo Branch of the National Cancer Institute of Genoa “M. Ascoli”. Cancer Hospital Center Palermo, ItalySearch for more papers by this authorROSARIA FARRUGGIO, ROSARIA FARRUGGIO Hormone Biochemistry Laboratories School of Medicine University of Palermo Palermo, ItalySearch for more papers by this authorCARMELA M. G. SORCI, CARMELA M. G. SORCI Hormone Biochemistry Laboratories School of Medicine University of Palermo Palermo, ItalySearch for more papers by this authorGIUSEPPA OLIVERI, GIUSEPPA OLIVERI Hormone Biochemistry Laboratories School of Medicine University of Palermo Palermo, ItalySearch for more papers by this authorROSALBA AMODIO, ROSALBA AMODIO Hormone Biochemistry Laboratories School of Medicine University of Palermo Palermo, ItalySearch for more papers by this authorMARCO DI FALCO, MARCO DI FALCO Hormone Biochemistry Laboratories School of Medicine University of Palermo Palermo, ItalySearch for more papers by this authorDOMENICO D'AMICO, DOMENICO D'AMICO Hormone Biochemistry Laboratories School of Medicine University of Palermo Palermo, ItalySearch for more papers by this authorLUIGI A. M. CASTAGNETTA, LUIGI A. M. CASTAGNETTA Hormone Biochemistry Laboratories School of Medicine University of Palermo Palermo, Italy Experimental Oncology and Molecular Endocrinology Units Palermo Branch of the National Cancer Institute of Genoa “M. Ascoli”. Cancer Hospital Center Palermo, ItalySearch for more papers by this author First published: April 1996 https://doi.org/10.1111/j.1749-6632.1996.tb16229.xCitations: 19 a This study was partially funded by the Italian Association for Cancer Research (AIRC) and by the National Research Council (CNR) Special Project “Aging” (Grant No. 95.01017.PF40). R. Farruggio and L. Comito hold grants from, respectively, the National Cancer Institute (IST) of Genoa and the Italian Association GROCTA. AboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Citing Literature Volume784, Issue1Basis for Cancer ManagementApril 1996Pages 70-84 RelatedInformation

We report that growth of LNCaP human prostate cancer cells is significantly stimulated (up to 120% above control) by physiological estradiol (E(2)) concentrations. This growth increase appears to be comparable to that induced by either testosterone or dihydrotestosterone, as also reported by others. This paper presents novel illustrative evidence for estrogen-binding proteins and messenger RNA transcripts in LNCaP cells. In fact, 1) the reverse transcriptase-polymerase chain reaction system documented normal messenger RNA for estrogen receptors (ER); 2) the radioligand binding assay allowed the detection of high affinity, reduced capacity binding sites in both soluble and nuclear cell fractions; and 3) the immunocytochemical analysis showed a consistently intensive staining for both ER and progesterone receptors. Compared to other human estrogen-responsive mammary cancer cells, MCF7 and ZR75-1, ER expression in LNCaP cells was not significantly lower, as shown by levels of the ER transcripts, number of sites per cell, or femtomoles per mg DNA as well as the percentage and intensity of immunocytochemical staining. A relative estimate of ER expression obtained by matching LNCaP with another human prostate cancer cell line, PC3, always displayed significantly and consistently higher levels in LNCaP cells. The detection of relatively high type I ER content in either cell compartment of LNCaP cells was paralleled by a highly intensive staining for progesterone receptors. In addition, evidence that the synthetic androgen R1881 did not compete for type I binding of E(2) and that any E(2)-induced growth was completely reversed by the pure antiestrogen ICI-182,780, but unaffected by the antiandrogen Casodex, clearly suggests that the biological response of LNCaP cells to E(2) is mediated via its own receptor.

Journal Article Canine leishmaniasis in western Sicily Get access Maria Dora Miceli, Maria Dora Miceli Cattedra di Clinica delle Malattie Tropicali e Sub-Tropicali, University of Palermo, Italy Search for other works by this author on: Oxford Academic PubMed Google Scholar S. Mansueto S. Mansueto Cattedra di Clinica delle Malattie Tropicali e Sub-Tropicali, University of Palermo, Italy Search for other works by this author on: Oxford Academic PubMed Google Scholar Transactions of The Royal Society of Tropical Medicine and Hygiene, Volume 81, Issue 1, January-February 1987, Page 175, https://doi.org/10.1016/0035-9203(87)90332-4 Published: 01 January 1987 Article history Accepted: 14 March 1985 Published: 01 January 1987

963 sera from contacts, persons from various localities, and blood donors were examined with a commercially produced kit for micro-immunofluorescence for the presence of antibodies to Rickettsia conorii. 10·6% of sera were serologically positive. The higher rates of positivity were observed in sera of contacts (19%) and persons from Mussomeli (20%) and Ustica (18·4%), the lower rates in blood donors from Palermo (3·5%). These results support the view that there is an occupational risk factor related to a rural environment.

The diagnosis of Boutonneuse Fever usually depends on clinical evidence (summer occurrence, fever, tache noire at the site of the tick bite, in 30-70% of cases, erythemato -papular rash, prompt response to chloramphenicol or tetracycline treatment). Serological confirmation is difficult since the only diagnostic procedure currently feasible, the Weil-Felix test, is not specific. Other more specific diagnostic procedures (agglutination, complement fixation, ELISA, indirect immunofluorescence tests) are beyond the possibilities of most laboratories (antigens are not available from the market). In the present paper, results obtained with a new commercially produced kit for indirect immunofluorescence are reported. Sera from patients with infectious and non infectious diseases as well as Boutonneuse Fever (at various stages of illness, from 6 days to 12 months) were examined. Sera from blood donors were also included. Specificity and sensitivity were satisfactory as well as reproducibility of results. Some apparently false positivities must be related to the present epidemiological pattern in western Sicily, and namely to the incidence of asymptomatic cases of Boutonneuse Fever, as demonstrated by recent works.

(1982). Counterimmunoelectrophoresis (CIEP) and ELISA tests in the diagnosis of canine leishmaniasis. Annals of Tropical Medicine & Parasitology: Vol. 76, No. 2, pp. 229-231.

The diagnosis of acute toxoplasmosis usually depends on serology, since clinical and/or histological features are difficult and/or often misleading. IgM titers are the best indicators of infection acquired in the past two to four months. IgG titers are generally correlated with non-active infections as well as previous (symptomatic and/or asymptomatic) illness. In the present paper, results obtained with a new kit for the evaluation of IgG and specific-IgM by micro-ELISA technique, are reported. Optical density values in sera from: a) blood donors; b) miscellany group; c) suspected toxoplasmosis, were at various degree high for IgG. Few sera of the entire sample (in the group of suspected toxoplasmosis and one in miscellany) showed high optical density for specific IgM. Reading of results with spectrophotometer were in agreement with reading to the naked eye. Reproducibility was satisfactory. Unfortunately some sera positive in the first determinations gave equivocal results in successive proofs. For these reasons diagnosis of toxoplasmosis must be based upon the use of at least three tests.