Showing papers by "University of Modena and Reggio Emilia published in 1991"

Acquired dyschromatopsia among styrene-exposed workers.

Abstract: We investigated the occurrence of color vision loss in 75 styrene-exposed workers and in 60 referents. Color vision was evaluated by adopting the Lanthony D 15 desaturated panel, a test specifically suited to detect mild acquired dyschromatopsia. The results of the test were expressed as Color Confusion Index. Styrene exposure was evaluated with both environmental and biological monitoring. Airborne levels of the solvent were 3.2 to 549.5 mg/m3. In styrene-exposed workers color vision was significantly impaired when compared with referents matched for age. A significative correlation was found between environmental and urinary levels of styrene and Color Confusion Index excluding the influence of age in multiple regression analysis, indicating the possibility of a dose-effect relationship. The findings suggest that styrene can induce an early appearance of a dose-dependent color vision loss.

Inhibin and activin modulate human monocyte chemotaxis and human lymphocyte interferon-gamma production.

Abstract: Inhibin and activin are referred to as gonadal glycoprotein hormones whose function is the control of FSH release from the pituitary gland. However, several observations indicate that inhibin and activin are produced in various organs and serve multiple functions. Because bone marrow and spleen produce inhibin and activin, our aim was to evaluate their possible effect on cell-mediated immune function. For this reason we studied 1) monocyte chemotaxis, 2) lymphocyte interferon-gamma production, 3) phytohemagglutinin-induced lymphocyte proliferation, and 4) nonmajor histocompatibility complex-restricted and lymphokine-activated lymphocyte cytotoxicity. All studies were performed on human peripheral blood cells in the absence or presence of various doses of inhibin, activin, or inhibin plus activin. A significant dose-related increase in monocyte chemotaxis was induced by inhibin. Activin increased the migrational activity of monocytes, but via random, not directed, migration. Inhibin significantly decreased interferon-gamma production, and its effect was reversed by activin. Inhibin and/or activin had no significant effect on either phytohemagglutinin-induced lymphocyte proliferation or lymphocyte cytotoxic capability. The present demonstration that inhibin and activin may affect some immune parameters suggests a possible involvement of these hormones in regulating cell-mediated immune function.

Leber's hereditary optic neuropathy: genetic, biochemical, and phosphorus magnetic resonance spectroscopy study in an Italian family.

Abstract: Three siblings of a family affected with Leber's hereditary optic neuropathy (LHON) showed a mitochondrial DNA mutation at position 11778. The lactate response to a standardized effort was increased in only one case. Muscle biopsies and biochemistry of muscle and platelet mitochondrial enzymes were normal. All patients showed an altered energy metabolism during exercise and during recovery after exercise on phosphorus 31-magnetic resonance spectroscopy (31P-MRS) of muscle. Brain 31P-MRS showed a decreased energy reserve (decreased PCr/Pi ratio) in all patients. 31P-MRS noninvasively demonstrated an altered mitochondrial energy metabolism in muscle and, for the first time, in the brains of LHON patients.

ProMACE-cytaBOM versus MACOP-B in intermediate and high grade NHL. Preliminary results of a prospective randomized trial.

Abstract: One hundred seventy-nine patients with intermediate or high-grade non-Hodgkin's lymphoma were randomized to receive either ProMACE-CytaBOM (P-C) or MACOP-B (M-B). At last follow-up 71 patients in the P-C arm and 78 in the M-B arm were assessable for response. Forty-one patients treated with P-C (58%) and 49 patients treated with M-B (63%) achieved a CR. Moreover 18 and 22 patients achieved PR with P-C and M-B, respectively. Twenty-five patients relapsed, 12 in the P-C arm and 13 in the M-B arm. Thirty-nine patients died, 32 from disease progression, 5 from treatment related causes, and 2 from other causes. No differences between the two treatment groups were observed as regard to relapse or death-rate. At 27 months the survival rate was of 71.9% for patients treated with P-C and 70.7% for those treated with M-B. At 2 years the RFD rate was 64% and 60% for patients in P-C and M-B arm, respectively. Patients treated with M-B experienced an high rate of methotrexate-related toxicity. ProMACE-CytaBOM and M-B seem provided with similar activity. However P-C seem less toxic and more manageable in an outpatient setting.

Hepatocellular carcinoma: risk factors other than HBV.

Abstract: Experimental and epidemiological studies of risk factors for hepatocellular carcinoma (HCC): cirrhosis male sex oral contraceptives alcohol smoking and aflatoxins are evaluated with meta-analysis for oral contraceptives alcohol and smoking. It is likely that an initiating event and one or more promoting events interact probably with prolonged inflammation necrosis and regeneration to cause cancer in several types of cirrhosis. Over 90% of HCC patients have cirrhosis usually from hepatitis B virus. The viral post-necrotic liver is often chronically dysplastic but other types of cirrhosis are associated with HCC if they endure long enough. The proportion of men with HCC increases as hepatitis progressors to cirrhosis and then to HCC. Meta-analyses of 3 oral contraceptive studies resulted in a risk of 2.8 for 8 years. Population studies do not show any concentration of HCC in countries with high pill use so the rarity of this cancer may have biased the results. Large epidemiologic studies are needed to refine risk estimates for oral contraceptives and HCC. Alcohol abuse of >80 g/day gives a risk of about 1.65 in pooled studies compared to a risk of 1.1 for <80 g/day. Smoking gives a risk of 1.9 but there is no evidence for a secular trend by country in proportion to dose as is evident for lung cancer. There is good experimental evidence that aflatoxin acts as an initiator for liver cancer but there is not practical way to judge exposure for clinical studies.