Biomedical subjects
Publications and source records attributed to L Bianchi.
A case of hepatic aneurysm diagnosed by duplex-Doppler US is reported. The demonstration of a complex hepatic hiliar mass with an arterial turbulent blood flow spectrum, permitted the diagnosis, which was confirmed by subsequent abdominal CT exploration. Our case confirms that duplex-Doppler US is useful non-invasive tool for the diagnosis of hepatic artery aneurysm.
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The aim of our study was to elucidate further possible genetic influences on the incidence and progression of alcoholic liver disease. We determined HLA A, B and DR antigens in a well-controlled group of chronic alcoholics with and without liver disease, in repeated liver biopsies over period of 8.1 years (+/- 0.4 SEM). Patients with the antigen B 35 had an increased incidence of alcoholic liver cirrhosis, and especially a more rapid progression to cirrhosis (p less than 0.01). Increased susceptibility of these patients was shown by a more rapid progression of liver disease, despite the consumation of less alcohol over a shorter period. Results of this long-term study suggest that there is a sub-group of alcoholics genetically predisposed to higher susceptibility with more rapid deterioration of alcohol-induced liver disease.
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To evaluate the influence of chronic alcohol consumption on the cellular immune system in man, we investigated the immune response to seven intradermally applied common antigens and in vitro stimulation of peripheral lymphocytes by Phytohemagglutinin A and concanavalin A in chronic alcoholics with (n = 15) and without (n = 15) liver disease. The results suggest that the diminished cellular immune response in chronic alcoholics is not primarily a direct sequel to alcohol consumption; it is more likely that the impaired immune response is linked to severity of the liver damage itself and to malnutrition.
In this long-term follow-up evaluation of chronic alcoholics without established cirrhosis we investigated the influence of alcohol on the progression of fibrosis and the prognostic significance of histological features. We were unable to confirm results of retrospective cross-sectional analysis suggesting a linear relationship between alcohol intake and the development of cirrhosis. Alcoholic hepatitis, advanced fibrosis, central hyaline necrosis and central vein sclerosis were unfavorable signs for the further course of the disease. All but one of the patients with central vein sclerosis who progressed to advanced fibrosis also had an alcoholic hepatitis in one of their biopsies. Two patients had an acute alcoholic hepatitis initially, and later showed the mixed histological pattern of an alcohol-induced chronic active hepatitis, a pattern which was also seen in four other patients, all progressing to cirrhosis. This may be taken as evidence that immunological factors contribute in some patients to progression of fibrosis.
In a retrospective study 157 liver specimens from hemophiliac patients (105 percutaneous needle and 12 wedge biopsies, 40 autopsy specimens) were read blindly and independently by four pathologists on the basis of a computer codable questionnaire asking for evaluation of individual histologic features, classification of the liver disease, and speculation on etiology. The majority of cases had histologic evidence of mild chronic viral hepatitis; 7.6% of all cases were classified as CAH, and an additional 7.6% as CPH by all four interpreters. A large number (40.8%) were on the borderline of CAH and CPH or CLH. These were classified as "possible CAH" because of a diagnosis of CAH by one to three of the pathologists. Although there was therefore some interobserver variability in the diagnostic labels applied to these cases, all four pathologists were strikingly similar in their identification of individual histologic features. Furthermore, on blind rereadings, each pathologist made the same diagnosis in more than 90% of readings. In this retrospective study, serologic data were not available in many cases. Thus, etiologic considerations were based purely on speculation from the histologic appearance. One case was identified as "definite" and 28 of 157 (18%) as "possible" HBV infection. Based on the assumption that some of the individual histologic criteria indeed might be in favor of NANB hepatitis, 21 cases (13%) were considered "definite" NANB, and "possible" NANB was suspected in 107 additional cases (68%). The addition of these figures makes clear that within the limitations of histologic assessment, double infections appear to be frequent in this setting.(ABSTRACT TRUNCATED AT 250 WORDS)
The effects of L-641,953 (R-8-fluoro-dibenzo[b, f]thiepin-3-carboxylic acid-5-oxide) have been studied on pulmonary and other smooth muscle preparations in vitro and in vivo. When studied in vitro on guinea-pig tracheal chains, L-641,933 produced significant shifts in the dose-response curves to the prostaglandin endoperoxide analogues, U-44069 (pA2 7.06) and U-46619 (pA2 7.14), and prostaglandin (PG) F2 alpha (pA2 6.33) had minimal activity against contractions induced by histamine (pA2 4.38), 5-hydroxytryptamine (pA2 4.63), and acetylcholine (pA2 4.56) and slightly enhanced relaxation induced by PGE2. When tested on the guinea-pig gall bladder strip in vitro, L-641,953 antagonized contractions induced by U-44069 (pA2 7.03) but was less active against those induced by PGF2 alpha (pA2 6.03), PGE1 (pA2 5.62), and histamine (pA2 4.84). When tested in vitro on the guinea-pig pulmonary artery, L-651-953 significantly antagonized contractions induced by U-44069 (pA2 7.04), U-46619 (pA2 7.14), and PGF2 alpha (pA2 7.16) but was less effective against contractions induced by histamine (pA2 4.19). Schild analysis indicated that L-641,953 was fully competitive against contractions of either the guinea-pig tracheal chain induced by U-46619 or the guinea-pig pulmonary artery induced by U-44069 and U-46619. When tested on human platelets in vitro L-641,953 inhibited aggregation induced by U-44069 (IC50 1.3 X 10(-6) M) but not ADP.(ABSTRACT TRUNCATED AT 250 WORDS)
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To study the effect of ultraviolet light (UVL) exposure on the pathogenesis of vesiculobullous lupus erythematosus (VBLE), the back of depilated Strain 2 female guinea pigs was injected with sera from 2 patients with VBLE, 3 patients with non-bullous systemic lupus erythematosus (SLE) (disease control) and 4 normal human adults (normal control). Normal saline was also used as an additional control. Of the 20 injected areas, only half (10) were then irradiated with one minimal erythema dose of UVB (310 nm). The clinical and histologic features of the areas injected with VBLE sera and then irradiated showed significant differences from the areas only injected, as well as from the areas receiving injection and irradiation of the control sera (both disease and normal). Immunofluorescence studies, on the other hand, showed similar results in the areas injected with either VBLE or SLE sera. These results suggest that the most likely mechanism for induction of VBLE blisters is photoactivation of circulating factor(s) that damage the dermoepidermal junction of both sun-exposed and non-sun-exposed skin.
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We have isolated a thermosensitive mutant which is transformed into a population of cells devoid of mitochondrial DNA (rho 0 cells) at 35 degrees C and is deficient in mitochondrial (mt) DNA polymerase activity. A single recessive nuclear mutation (mip1) is responsible for rho 0 phenotype and mtDNA polymerase deficiency in vitro. At 25 degrees C (or 30 degrees C) a dominant suppressor mutation (SUP) masks the deficiency in vivo. The meiotic segregants (mip1 sup) which do not harbor the suppressor have a rho 0 phenotype both at 25 and 35 degrees C. They have no mtDNA polymerase activity, in contrast with MIP rho 0 mutants of mitochondrial inheritance which do exhibit mtDNA polymerase activity. In the thermosensitive mutant (mip1 SUP), the replication of mtDNA observed in vivo at 30 degrees C is completely abolished at 35 degrees C. In the meiotic segregants (mip1 sup), no mtDNA replication takes place at 30 and 35 degrees C. The synthesis of nuclear DNA is not affected. DNA polymerases may have replicative and/or repair activity. There is no evidence that mip mutants are deficient in mtDNA repair. In contrast the MIP gene product is strictly required for the replication of mtDNA and for the expression of the mtDNA polymerase activity. This enzyme might be the replicase of mtDNA.
To date, three types of NANBH have been distinguished by epidemiological, clinical and experimental data. We examined the liver biopsies of three patients with an acute NANBH resembling hepatitis A from the infection route, incubation period and clinical course. The liver biopsies revealed lesions with a portal and periportal predominance, thus also exhibiting parallels with hepatitis A on the histopathological level.
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