Interference study of the chi c0(13P0) in the reaction -pp-->pi0pi0.

Fermilab experiment E835 has observed (-)pp annihilation production of the charmonium state chi(c0) and its subsequent decay into pi(0)pi(0). Although the resonant amplitude is an order of magnitude smaller than that of the nonresonant continuum production of pi(0)pi(0), an enhanced interference signal is evident. A partial wave expansion is used to extract physics parameters. The amplitudes J=0 and 2, of comparable strength, dominate the expansion. Both are accessed by L=1 in the entrance (-)pp channel. The product of the input and output branching fractions is determined to be B((-)pp-->chi(c0))xB(chi(c0)-->pi(0)pi(0))=(5.09+/-0.81+/-0.25)x10(-7).

Occurrence and significance of IgG liver membrane autoantibodies (LMA) in chronic liver diseases of different aetiology.

The prevalence of liver cell membrane antibodies (LMA) was evaluated in the sera of 124 untreated patients with various chronic liver diseases, in 17 acute hepatitis patients and in 40 normal controls by indirect immunofluorescence on rabbit hepatocytes, isolated by non-enzymatic method. The presence of LMA was compared with the presence of HBs Ag, anti-HBc and non-organ specific autoantibodies (anti-nuclear antibody, ANA; smooth muscle antibody, SMA; anti-mitochondrial antibody, AMA; liver-kidney microsomal antibody, LKM). LMA was found in 83% of autoimmune chronic active liver disease (CALD), in 47% of cryptogenic CALD and in 42% of primary biliary cirrhosis (PBC). LMA prevalence both in HBsAg positive and HBsAg negative/anti-HBc positive CALD was 11%, significantly lower than in the other three groups. In the cryptogenic group the prevalence of non-organ specific autoantibodies was significantly lower than LMA prevalence. The 35 LMA positive sera were titred to end point dilution. Autoimmune cases presented titres higher than those of all the other groups. Adsorption experiments showed that in autoimmune cases LMA fluorescence is not blocked by pre-incubation with liver antigens LSP and LP2, while a mild blocking effect was observed in some HBsAg positive cases or PBC sera. No cross-reaction with mitochondrial antigens was observed in PBC sera. LMA can still be considered a marker of autoimmune CALD only when present at high titre and without cross-reactivity with other liver antigens.

Hepatocyte membrane-bound IgG and circulating liver-specific autoantibodies in chronic liver disease: relation to hepatitis B virus serum markers and liver histology.

Hepatocytes isolated from 101 biopsies were examined for membrane-bound IgG. The sera of the patients were tested for anti-liver-specific lipoprotein by radioimmunoassay and for liver membrane autoantibody (by indirect immunofluorescence on isolated rabbit hepatocytes. The seven patients with normal liver or minor nonspecific alterations were negative for membrane IgG and serum antibodies. Membrane IgG with granular distribution was found in 41 patients [21 hepatitis B virus-related chronic active hepatitis (CAH), 3 cryptogenic CAH, 3 chronic persistent hepatitis, 6 prolonged viral hepatitis, 1 alcoholic cirrhosis, and 6 primary biliary cirrhosis]. Membrane IgG with linear fluorescence pattern was detected in 12 cases (4 autoimmune CAH, 3 HBsAg-positive CAH, 2 alcoholic cirrhosis, 1 anti-HBc positive CAH, 1 cryptogenic CAH, and 1 prolonged viral hepatitis). A strong association between granular IgG and serum HBsAg was found. Nuclear localization of IgG was found in 34 patients and correlated with the positivity of granular membrane IgG. The highest prevalence of anti-liver-specific lipoprotein was found in primary biliary cirrhosis and autoimmune CAH cases which were also positive for liver membrane autoantibody. No relationship was found between the presence of membrane IgG and circulating liver-specific autoantibodies. Membrane IgG and anti-liver-specific lipoprotein correlated with the presence of moderate and severe portal inflammatory infiltration but not with piecemeal necrosis or transaminase levels. Eleven of the twelve patients with linear membrane IgG presented chronic active liver disease with moderate to severe signs of liver damage. Therefore, it is suggested that, while granular membrane IgGs are related to hepatitis B virus, antigenic expression on the hepatocyte surface and/or the presence of immune complexes, linear membrane IgG could play a role in the immunopathogenesis of liver cell damage particularly in "autoimmune" cases which present high percentages of positive cells liver-specific autoantibodies.

[Effect of 2 mercaptopropionylglycine on the cytotoxic activity of lymphocytes from patients with chronic active hepatitis against rabbit hepatocytes isolated and cultured in vitro]. / Effetto della 2 mercaptopropionilglicine (2 MPG) sull'attività citotossica contro epatociti di coniglio isolati e coltivati in vitro dei linfociti di soggetti con epatite cronicaz attiva.

"In vivo" and "in vitro" action of 2 MPG on lymphocytotoxic activity was evaluated in 22 patients with CAH, 14 were HBsAg positive and 8 were negative. The test was performed with and without 2 MPG in the colture medium, and before and after treatment. HBsAg+ patients received 2 MPG treatment, while HBsAg- ones received immunosoppressive therapy and 4 of these were on 2 MPG treatment as well. Cytotoxic Index was reduced non-significantly by addition of 2 MPG in colture medium in both groups. 2 MPG treatment does not modify cytotoxic activity which is reduced by immunosoppressive therapy. These findings suggest a positive effect of 2 MPG on liver-cell metabolism with an increased resistence of the epatocyte to the "in vitro" lymphocytes aggression. Hence it may be suggested an association treatment with immunosoppressive agents and 2 MPG.