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C Liguori

Publications and source records attributed to C Liguori.

26 records · Page 2Linked to original sources
PubMed1985

Occurrence of cell death (apoptosis) during the involution of liver hyperplasia.

A single intravenous injection of lead nitrate at a dose of 10 mumoles/100 gm of body weight caused liver enlargement associated with hepatic cell proliferation. In the present study the involution of liver hyperplasia which follows the withdrawal of lead was studied in male Wistar rats. Histologic examination of liver sections from rats killed during the regression of the liver did not show any sign of massive lytic cell necrosis; no variation in the levels of serum glutamate pyruvate transaminase could be observed during the same time period; however, light microscopic observation of sections from the involuting liver showed the presence of several apoptotic bodies; the occurrence of apoptotic bodies was also confirmed by ultrastructural examination. Their incidence was found to be markedly increased at 5 days after treatment, a time period when the liver is already regressing; very few apoptotic bodies were observed in control animals or in treated rats 2 days after lead injection, a time point when mitotic index reached its maximum, or at 15 days, when the liver had returned to control values. These findings suggest that removal of excess liver which follows the initial hyperplasia caused by lead is due to a controlled mode of cell death, namely, apoptosis.

Alanine Transaminase↗
PubMed1984

Stimulation of DNA synthesis after a single administration of cadmium nitrate.

The effect of a single intravenous (i.v.) injection of cadmium nitrate was investigated in livers of male Wistar rats. A significant increase in liver weight, accompanied by an elevation of total hepatic DNA content was observed. DNA synthesis as measured by the incorporation of [3H]thymidine, was found to be 6 times greater than the control, at 24 h after treatment, and remained elevated over a period of 72 h. This elevation in DNA synthesis was not a consequence of cell necrosis, since no increase of serum glutamate-pyruvate transaminase (SGPT) activity was observed.

Alanine Transaminase↗
PubMedDate not supplied

Uneven copper distribution in the human newborn liver.

The pattern of copper distribution in human newborn liver was investigated by histochemical methods (rhodamine, orcein and rubeanic acid) and by atomic absorption spectroscopy. A significant correlation (p less than 0.005) was found between the degree of histochemical positivity and the copper concentration found by atomic absorption spectroscopy. In the majority of the 30 livers examined (first group), the copper concentration was much higher than that of normal adult liver, although exhibiting striking individual differences. No correlation between the copper content and sex, body weight or gestational age was found. From a second group of five livers, longitudinal tissue slices 0.5 cm thick were partitioned into regular blocks of about 0.5 gm, which were individually analyzed by atomic absorption spectroscopy. Copper appeared unevenly distributed within each liver, with marked differences even between adjacent blocks. However, a consistent tendency of copper to accumulate in the left lobe more than in the right one was evident. Five additional blocks, one for each liver, were further partitioned into 10 small specimens of a final size (0.05 gm), comparable to that of a needle biopsy. Even at this sampling level, consisting of tissue fragments taken from a small tissue area, the copper concentration appeared quite irregularly distributed. These findings may be considered for two different aspects: (a) the biological implications of the pattern of copper accumulation in different lobar and lobular liver compartments and (b) the statistical inference, for diagnostic purposes, of the mean liver copper content from measurements of single percutaneous biopsy specimens.

Age Factors↗
PubMedDate not supplied

Hepatic expression of hepatitis B and delta virus antigens in patients with acute and chronic hepatitis.

Delta antigen (delta-Ag), hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg) were examined by immunofluorescence and immunoperoxidase staining in 106 deparaffinized liver biopsy samples from HBsAg-positive patients with acute and chronic hepatitis. The delta-Ag was present in 15 cases (14%), with nuclear positivity varying greatly in intensity and prevalence. Patients with chronic hepatitis associated with delta infection had a histological picture characterized by foci of intralobular inflammation, many apoptotic bodies and shrunken hepatocytes with no satellite signs of inflammation. The histological pattern of delta antigen-positive acute hepatitis was characterized by the presence of a large number of intralobular apoptotic bodies. The inflammatory reaction mainly involved the portal tracts with piecemeal necrosis, but without collagen production. In the same cases the pattern of expression of HBsAg and HBcAg was unusual: in three cases HBcAg and HBsAg were concomitantly present, whereas in one case none of the hepatitis B virus markers was detectable.

Acute Disease↗
PubMedDate not supplied

Expression of ATP7B in normal human liver.

ATP7B is a copper transporting P-type ATPase, also known as Wilson disease protein, which plays a key role in copper distribution inside cells. Recent experimental data in cell culture have shown that ATP7B putatively serves a dual function in hepatocytes: when localized to the Golgi apparatus, it has a biosynthetic role, delivering copper atoms to apoceruloplasmin; when the hepatocytes are under copper stress, ATP7B translocates to the biliary pole to transport excess copper out of the cell and into the bile canaliculus for subsequent excretion from the body via the bile. The above data on ATP7B localization have been mainly obtained in tumor cell systems in vitro. The aim of the present work was to assess the presence and localization of the Wilson disease protein in the human liver. We tested immunoreactivity for ATP7B in 10 human liver biopsies, in which no significant pathological lesion was found using a polyclonal antiserum specific for ATP7B. In the normal liver, immunoreactivity for ATP7B was observed in hepatocytes and in biliary cells. In the hepatocytes, immunoreactivity for ATP7B was observed close to the plasma membrane, both at the sinusoidal and at the biliary pole. In the biliary cells, ATP7B was localized close to the cell membrane, mainly concentrated at the basal pole of the cells. The data suggest that, in human liver, ATP7B is localized to the plasma membrane of both hepatocytes and biliary epithelial cells.

Adenosine Triphosphatases↗