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PubMed2006

The role of bright liver echo pattern on ultrasound B-mode examination in the diagnosis of liver steatosis.

AIM: The observation of bright liver echo pattern on ultrasound is commonly considered a sign of hepatic steatosis. However, the interference of liver fibrosis on sensitivity and specificity of bright liver echo pattern has caused many to question its effectiveness as a diagnostic tool. The objective of this study was to evaluate the sensitivity, specificity and predictive values of bright liver echo pattern for liver steatosis. PATIENTS AND METHODS: We studied 235 consecutive patients suspected of having liver disease of various aetiologies. Median age was 52 years (range, 17-72 years), and there was a male/female ratio of 1:18. All patients underwent ultrasound examination before liver biopsy and was performed by two operators. The presence or absence of bright liver echo pattern and posterior attenuation or areas with different patterns of fat infiltration were noted. Histologic evaluation was performed and graded by Ishak score. Steatosis was categorised as absent, 0-2%, 3-29% to 30-49% or >50%. RESULTS: Interobserver concordance was high. Bright liver echo pattern was found in 67% of patients with steatosis of any degree and 89% of patients with steatosis of >or=30%. Only three patients without steatosis, who had a low Ishak score, demonstrated bright liver echo pattern on ultrasonography. The sensitivity, specificity, positive predictive value and negative predictive value of bright liver echo pattern for steatosis were 64%, 97%, 96.0% and 65%, respectively. Among the subgroup of patients who had steatosis of >or=30%, the sensitivity, specificity, positive predictive value and negative predictive value of bright liver echo pattern were 91%, 93%, 89% and 94%, respectively. The sensitivity, specificity, positive predictive value and negative predictive value of posterior attenuation and/or skip areas associated with bright liver echo pattern for steatosis were 89.7%, 100%, 100% and 92.3%, respectively. Univariate analysis showed bright liver echo pattern to be associated only with steatosis and not with fibrosis. CONCLUSION: We concluded that the presence of bright liver echo pattern is a sign of liver steatosis and that liver fibrosis does not interfere with ultrasound measurements. Posterior attenuation and/or skip areas are closely related to steatosis of >or=30%.

Adolescent↗
PubMed1997

Morphology of liver stellate cells and liver vitamin A content in 3,4,3',4'-tetrachlorobiphenyl-treated rats.

BACKGROUND/AIMS: Because xenobiotics decrease the vitamin A stores localized in the liver stellate cells, we investigated morphological alterations in the liver of rats exposed to 3,4,3',4'-tetrachlorobiphenyl. Special attention was given to the morphology of the liver stellate cells and to their relationship to the liver vitamin A content. METHODS: Six rats received an intraperitoneal injection of 3,4,3',4'-tetrachlorobiphenyl (300 mumol/kg) in soyabean oil. A further six rats received the vehicle alone. After 7 days, all rats were killed and their livers assayed for vitamin A. Liver stellate cells were examined and counted on liver sections, stained with toluidine blue or immunocytochemically for desmin and, for some animals, for alpha-smooth muscle actin. RESULTS: In the livers of 3,4,3',4'-tetrachlorobiphenyl-treated rats, we found spotty and bridging necrosis, with inflammation and accumulation of desmin-positive liver stellate cells. Steatosis and mild portal inflammation were also observed. 3,4,3',4'-Tetrachlorobiphenyl decreased the liver vitamin A content by 38%, whereas morphometric analyses showed a 40% decrease of the number of toluidine blue-detected liver stellate cells and an 11% increase of desmin-detected liver stellate cells, indicating a likely differentiation of liver stellate cells into myofibroblast-like cells. 3,4,3',4'-Tetrachlorobiphenyl treatment did not modify the expression of alpha-smooth muscle actin. Morphological alterations were more pronounced in periportal than in pericentral areas. The liver vitamin A content was positively correlated (r = 0.56, p < 0.005) with the number of toluidine-blue detected liver stellate cells. CONCLUSIONS: 3,4,3',4'-tetrachlorobiphenyl administration results in an accumulation of liver stellate cells that start differentiating into myofibroblast-like cells. The 3,4,3',4'-tetrachlorobiphenyl-induced decrease in liver vitamin A probably results from this differentiation, although other mechanisms cannot be excluded.

Animals↗
PubMed1999

Effects of Sho-saiko-to extract on liver fibrosis in relation to the changes in hydroxyproline and retinoid levels of the liver in rats.

To examine the effects of Sho-saiko-to extract on liver fibrosis, the drug was administered to rats with dimethylnitrosamine-induced liver-injury at various doses. Hydroxyproline and retinoid levels in the liver were measured as indicators of liver function. In liver-injured rats, the hydroxyproline level in the liver (957+/- 154nmol g(-1)) was about 4.16-times that found in normal liver (230+/-11 nmol g(-1)), but administration of Sho-saiko-to extract (0.75%, 1.5% or 3%) reduced the hydroxyproline level significantly (554+/-58, 356+/-51, 374+/-66nmol g(-1), P<0.01). Single administration of the active constituents of Sho-saiko-to extract, glycyrrhizin, baicalin or baicalein, decreased the hydroxyproline level significantly compared with the ordinary food group (P < 0.05), but the decrease was smaller compared with the Sho-saiko-to extract group. The liver retinoid level was higher in the Sho-saiko-to extract group than the ordinary food group and the value increased dose-dependently. A significant negative correlation, r=-0.814 (P<0.001) was detected between the hydroxyproline level and retinoid level in the liver of liver-injured rats. Significant negative correlations, r =-0.728 (P < 0.001) and r= -0.873 (P < 0.001), were also detected between the liver hydroxyproline level and the liver concentrations of the active constituents (glycyrretic acid, baicalin and baicalein) in the liver-injured rats. From these findings, it was considered that the liver concentrations of hydroxyproline and retinoid as well as the active constituents were involved in the improvement of liver fibrosis in the liver-injured rats administered Sho-saiko-to extract. Administration of Sho-saiko-to extract inhibited collagen production while an increase in retinoid level inhibited activation of Ito cells leading to inhibition and prevention of liver fibrosis.

Administration, Oral↗
PubMed1989

Reduced-size orthotopic liver transplantation: use in the management of children with chronic liver disease.

Reducing the size of a liver for use in a recipient smaller than the donor is one way to reduce mortality before orthotopic liver transplantation in children because of the scarcity of pediatric organ donors. In this report, we review the results of this approach over the past 2 years, during which we have used reduced-size orthotopic liver transplantation routinely in small children. Forty-nine children underwent orthotopic liver transplantation between September, 1986, and October, 1988; orthotopic liver transplantation with a whole organ (full-size orthotopic liver transplantation) was performed in 36 children, whereas 13 patients received reduced-size orthotopic liver transplantation. In two pairs of patients, the reduced grafts were obtained from single donors, using a "split-liver" procedure. All grafts were implanted in the orthotopic position following total recipient hepatectomy. The preoperative diagnostic categories were not significantly different between groups. Patients receiving reduced-size orthotopic liver transplantation were younger (1.6 +/- 1.5 vs. 4.4 +/- 4.6 years), and a higher percentage were in the intensive care unit prior to transplant (31 vs. 9%). Thirty of 36 (82%) patients receiving full-size orthotopic liver transplantation and 10 of 13 (77%) patients receiving reduced-size orthotopic liver transplantation are alive 3 to 27 months after transplantation. The rates of retransplantation were 24% for full-size orthotopic liver transplantation and 15% for reduced-size orthotopic liver transplantation. Despite the greater complexity of reduced-size orthotopic liver transplantation and the higher frequency of critically ill recipients selected for the procedure, the results of reduced-size orthotopic liver transplantation are comparable with full-size orthotopic liver transplantation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1998

The portal lobule in rat liver fibrosis: a re-evaluation of the liver unit.

We re-evaluated three schemes of liver organization: the classic lobule, the portal lobule, and Rappaport's liver acinus. The lobular angioarchitecture of normal rat liver and the three-dimensional structure of pseudolubules found in rat livers with fibrosis induced by swine serum were compared with the classic lobule of the pig. Normal and fibrotic rat livers and pig livers were perfused, injected with either India ink or 0.75% OsO4 through the portal and/or hepatic vein, and immersionfixed. Whole lobes and hand-cut thick sections were made transparent with a solution of benzyl benzoate and methyl salicylate. The angioarchitecture of normal rat liver differs from pig liver. In the former, terminal portal branches and central veins interdigitate, and in the latter, numerous terminal portal branches that arise from interlobular portal veins establish a vascular basket surrounding one central vein and forming classic lobule. The structure of liver acinus is never found in the pig liver. The terminal portal branch, together with the terminal hepatic artery and bile duct, are present inside each pseudolobule of fibrotic rat livers. Blood from the terminal portal branch flows through inlet venules into radiating sinusoids, and, at the periphery converges into newly formed septal and angular outlet venules; these venules terminate in fibrotic central veins located at each corner. Pseudolobules are not rugby ball-like as Rappaport's liver acini are but are polyhedron in shape. The rat pseudolobules are comparable with the portal lobule; its structure and microcirculation are the reverse of the pig classic lobule. Rat pseudolobules are different from liver acini, as shown by the following: 1) their three-dimensional shape is different; and 2) they have a reverse relationship to classic lobules while acini are defined to subdivide classic lobules. In normal and fibrotic rat livers, the liver unit is the portal lobule with a terminal portal branch as the axial branch and central veins at the periphery. The co-existence of liver acini and classic lobules is doubtful.

Animals↗
PubMed1999

Ex vivo liver perfusion with arterial blood from a pig with ischemic liver failure.

To simplify liver support using an ex vivo perfused liver, an isolated pig liver was perfused with arterial blood from the recipient pig while monitoring the metabolic capacity of the ex vivo perfused liver. It was possible to perfuse the isolated liver for more than 24 h using arterial blood from a pig with ischemic liver failure. The viability of the isolated liver during support from the liver failure pig was well maintained as evidenced by the high adenylate energy charge (0.815) and a constant ketone body ratio (KBR) of over 1.0 sampled from the hepatic vein. Oxygen consumption (mean, 29.0 microl/min/g of liver) and bile production (mean, 24.2 microl/h/g of liver) were significantly higher in the isolated liver connected to the liver failure pig than in the organ connected to the pig without liver failure (15.5 microl/min/g and 7.3 microl/h/g, respectively). These findings suggest that this liver support system has sufficient metabolic capacity to support a failed liver. Further studies may provide the experimental basis necessary for the clinical application of this device in treatment of patients with acute liver failure.

Animals↗
PubMed2006

Doppler sonographic evaluation of hemodynamic changes in colorectal liver metastases relative to liver size.

OBJECTIVE: The mechanisms of hemodynamic alterations in colorectal liver metastases are not clearly understood yet. Considering that an increase in liver size in patients with metastases could also result in an alteration in total liver flow, we aimed to analyze hemodynamic changes relative to the liver volume and to search for the possibility of any intrinsic factors affecting blood flow in patients with metastases. METHODS: Twenty-eight patients with colorectal liver metastases and 20 control subjects with no liver disease were evaluated sonographically. All patients were examined prospectively by Doppler sonography and helical computed tomography. Hepatic hemodynamic parameters, including blood flow in the hepatic artery and portal vein, total blood flow to the liver, and Doppler perfusion index, were calculated, and values relative to liver volume were obtained. Hepatic perfusion changes in liver metastases were then compared with those in a control group. RESULTS: The liver volume of the patients with liver metastases was greater than that of the control group (P=.003). Hepatic arterial blood flow rates were higher, whereas portal flow rates were lower, in patients with liver metastases compared with control subjects (P<.05). Total liver blood flow was not significantly different between the two groups. However, total blood flow relative to liver volume was significantly lower in the metastatic group (P<.001). Doppler perfusion index values in the patients with metastasis were significantly higher than in the control group (P=.000). CONCLUSIONS: Our findings may support the hypothesis that a humoral mediator-induced portal venous flow reduction causes perfusion changes in liver metastases from colorectal disease. However, an additional intrinsic hepatic hemodynamic event should also be present. Doppler perfusion index measurements can provide additional information in the evaluation of patients with colorectal liver metastases.

Adult↗
PubMed1993

Dynamics of normal and injured human liver regeneration after hepatectomy as assessed on the basis of computed tomography and liver function.

We compared liver volume and function kinetics after partial hepatectomy according to extent of resection and severity of coexisting liver disease in 57 adults with uneventful postoperative courses. Liver volume and massiveness of resection, or resection rate, were estimated on computed tomography. Patients were categorized into three groups on the basis of reaction rate: small (< 30%), medium (30%-50%) and large (> 50%). The regenerative patterns of normal livers in the medium and large groups consisted of three phases: a rapid increase during the first month, some decrease in the second month and a final, slower increase. This contrasted with the pattern of injured livers with chronic hepatitis or cirrhosis, which generally showed a phase of less rapid, gradual increase. The regeneration rate (volume gain, cm3/day) during the first month was found to be proportional to resection rate in the presence or absence of liver disease. Normal livers regenerated at least twice as rapidly as injured livers in patients with comparable resection rates. Normal livers reached plateau levels within 1 to 2 mo regardless of the massiveness of resection, whereas regeneration took 3 to 5 mo in injured livers. Liver function (albumin, bilirubin) recovered concomitantly with liver volume in the medium group, whereas in the large group they generally returned to their initial values behind volume restoration, particularly in cirrhotic patients. In conclusion, human liver regeneration is strongly influenced by the massiveness of the resection and presence of coexisting liver disease. However, we found that some cirrhotic livers can regenerate, albeit more slowly and less completely, as long as the extent of hepatectomy remains within safe functional limits.

Adult↗
PubMed1968

[Studies On The Transmissibility Of Pathogenic-Organisms To Liver By Migrating Larvae Of Liver Fluke And Hookworm]

In order to confirm whether the migrating larvae of parasites could carry pathogenic organisms into liver and cause hepatitis, a series of experiments has been carried out. A. Clonorchis sinensis: Recovery rate of larvae in the abdominal cavity of rabbits: One to seven days after the administration adolescariae were recovered from the abdominal cavity in less than l % of the total number of metacercariae given. Generally, 1~6 larvae were found from each animal which was given 900~1,000 metacercariae, though many larvae were already found in the common bile ducts or remained still in intestine. Fate of Clonorchis sinensis in abdominal cavity: The young or mature worms which were introduced directly into the abdominal cavity were examined l5, 32, 40 and 42 days after the inoculation. Several larvae were found on the surface of liver in four animals. All the worms on the surface of the liver were dead and the biopsied liver tissues on the area where the worms were attached showed no pathological changes. Two of them were between bile duct and liver tissue but pus cell infiltration surrounding them was observed. In every case, pus cell infiltration was found in the peripheral portion of the liver and pus nodules on the surface of intestine and mesentery. The nodule in the intestinal wall contained the eggs of Clonorchis sinensis. Two worms in the abdominal cavity were still alive. From the above results it is suggested that the larvae of Clonorchis sinensis were capable of penetrating the intestinal wall and reaching the organs in the abdominal cavity and surviving for l5~42 days, but they were unable to penetrate the organs. No bacterial flora appeared from the lesion by culture method. Fate of Clonorchis sinensis which was inoculated into the peripheral region of liver: Small abscess was observed at the same area. Microscopically, the area became edematous and the vessels in the peripheral region were dilated. The parasites became necrotic and amorphous. Pathologically the lesions appeared as eosinophilic masses and neutrophile leukocytes were infiltrated surrounding the masses. In some cases, the dead worms were found apart from the original place of inoculation but no leukocyte infiltration was found. There was linear infiltration between the original site and the portion where the dead worm was found. The distance from the capsule varied from 0 to 4 mm. Sometimes, the eggs of Clonorchis sinensis were also found. In all cases, there were no living worms in liver tissues and hepatic ducts. In all case,. the bacteriological examination was negative. Do clonorchis sinensis transfer the microorganism? Five adult worms of clonorchis sinensis were incubated in the saline solution containing Staphylococcus aureus. The intestinal contents of these worms were cultured in the Nutient-agar plate and examined by Methylene Blue and Gram's stain. The area of liver tissue where the Clonorchis sinensis were inoculated showed no inflammatory changes after the 3 days of inoculation but no living Staphylococcus aureus was found in the culture media with which the pieces of liver tissues were smeared. B. Hookworm: Cutaneous infection: Four to eight days after the cutaneous infection of Ancylostoma caninum, the mice were sacrificed. Grossly, there was no abnormal finding in liver. The pieces of liver tissues were smeared on the Nutrient-agar plate, and cocci were found in four out of six examined. The microorganism were confirmed as the same species of Diplococcus pneumoniae which were grown in the hookworm culture media. Oral infection: 1,000 filariform larvae of Ancylostoma caninum were given orally. 24 hours later, the mice were sacrificed and the pieces of liver tissue were smeared on the Nutrient-agar plate. After 50 hours at 36 C, the bacterial colonies were examined bacteriologically. Staphylococcus albus was found from two out of four samples. Grossly there was no abnormality on the surface of liver, but microscopically there were spots like microabscesses which were infiltrated by leukocytes. The larvae were also found from other portions of liver tissues and they were surrounded by yellow colored material. In another experiment, a combination of Ancylostoma duodenale and Staphylococcus aureus was fed to mice. The mice sacrificed five days after the oral administration of Ancylostoma duodenale cultivated in the media containing Staphylococcus aureus. The liver pieces were examined routinely. The larvae cultivated in normal tap water which contained no Staphylococcus aureus was used as control. In the experimental mouse, the cocci appeared in the liver. Pathologically, microabscesses infiltrated with neutrophile leukocytes were found, but there was no manifestation of inflammatory change due to Staphylococcus aureus. There was only mechanical trauma due to the larvae penetration. Haemorrhage appeared only where the larvae were found.

Journal Article↗
PubMed2005

Liver regeneration and splenic enlargement in donors after living-donor liver transplantation.

Liver regeneration after donor hepactectomy offers a unique insight into the process of liver regeneration in normal livers. As the liver restores itself, concurrent splenic enlargement occurs. There are many theories about why this phenomenon takes place: some investigators have proposed a relative portal hypertension that leads to splenic congestion or, perhaps, the presence of a common growth factor that induces both the liver and spleen to enlarge. Between the months of June 2001 and May 2004, 112 live donor liver transplants (LDLTs) were performed in Chang Gung Memorial Hospital, Kaohsiung, Taiwan. The total number of donor hepatectomies performed during this period was 113, however, because one of the cases required dual donors. Of our 113 donors, we eventually analyzed the data of 109; 4 patients were lost to follow-up 6 months later and were excluded from our study. The average age of our donor population was 32.32 +/- 8.48 years. The mean liver volume at donation was noted to be 1207.72 +/- 219.95 cm3, and 6 months later, it was 1027.18 +/- 202.41 cm3. Expressed as a percentage of the original volume, the mean liver volume 6 months after hepatectomy was 90.70% +/- 12.47% in this series. For right graft donors, mean liver volume after 6 months was 89.68% +/- 12.37% of the original liver volume, whereas that for left graft donors was 91.99% +/- 12.6%. Only 26 of the 109 (23.85%) donors were able to achieve full regeneration 6 months post-donation. Notably, liver function profiles of all donors were normal when measured 6 months after operation. The average splenic volume at donation as measured by computed tomography (CT) volumetry was 159 +/- 58 cm3, and the splenic volume 6 months post-donation was 213 +/- 85 cm3. There was a mean increment in splenic volume of 35% +/- 28% 6 months after donation. The blood profiles of the donors were monitored; particular attention was given to platelet levels and liver function tests, and these were found to be within normal limits 6 months after operation. Of note, splenic enlargement was significantly greater among right-sided donors than their left-sided counterparts. Greater splenic enlargement was also observed in those donors who achieved full liver regeneration at their evaluation 6 months postoperatively than in those who did not. Although original liver volume was not re-established in most patients 6 months after liver donation, there seemed to have been no untoward effects to the donor. The factors that affect liver regeneration are complex and myriad. Although there is splenic enlargement at 6 months post-donation in donors of LDLT, there are no untoward effects of this enlargement.

Adult↗
PubMed2005

The influence of spleen size on liver regeneration after major hepatectomy in normal and early cirrhotic liver.

BACKGROUND/PURPOSE: The relationship between liver regeneration and spleen size after major hepatectomy in normal and cirrhotic liver was studied by single photon emission computed tomography (SPECT). MATERIALS AND METHODS: Twenty-six patients, 18 patients with normal liver and eight patients with cirrhotic liver, receiving major hepatectomy were included. Liver and spleen volumes were measured by SPECT before major hepatectomy, 6 months, 1 year and 2 years after operation. The correlation of liver and spleen volume during liver regeneration was analyzed. RESULTS: In both groups, the residual liver volume increased within the first year and decreased in the second year. No difference in regeneration ability was found. The spleen volume in cirrhotic liver was increased, with a trend similar to normal liver during the first year. In contrast, the increased spleen volume persisted up to the second year in cirrhotic patients. Age per year, the female sex, and body surface index had a positive correlation with increased percentage of liver volume. The spleen volume per 100 ml with time played a significantly negative role in increasing percentage of liver volume, confidence interval: -2.16 to -27.92, P=0.011. CONCLUSION: In early cirrhotic liver within normal functional limits, the liver still could regenerate as a normal liver after major hepatectomy in 1 year. Age, the female sex, and body surface index had positive correlation but the size of spleen volume played a negative role to regenerative liver volume.

Adult↗
PubMed2005

[Relationship between liver mass and soluble intercellular adhesion molecule-1 in patients with liver cirrhosis].

OBJECTIVE: To investigate the relation of liver mass to, liver hymodynamics and soluble intercellular adhesion molecule-1 in patients with liver cirrhosis. METHODS: The liver mass was measured by liver biopsy, hepatic hemodynamics by ultrasonography, and the contents of hyalurionic acid (HA), human procollagen III (HPC III) and collagen type IV (C IV) by radioimmunoassay in 100 patients with liver cirrhosis in compensation stage and 30 normal control subjects. RESULTS: Greater liver mass was accompanied by more severe liver fibrosis and reduced liver blood flow. The contents of HA, HPC III and C IV were obvious higher in the patients than in the normal controls (P<0.05) and increased with the liver mass. The liver mass was positively related to serum liver fibrosis indices (r=0.5612, P<0.05). CONCLUSION: Liver mass in patients with liver cirrhosis is related to hepatic hemodynamics, indices for liver fibrosis and liver pathology.

Aged↗
PubMed2005

Effects of tocotrienols on cell viability and apoptosis in normal murine liver cells (BNL CL.2) and liver cancer cells (BNL 1ME A.7R.1), in vitro.

The effects of tocotrienols on murine liver cell viability and their apoptotic events were studied over a dose range of 0-32 microg mL(-1). Normal murine liver cells (BNL CL.2) and murine liver cancer cells (BNL 1ME A.7R.1) were treated with tocotrienols (T(3)), alpha tocopherol (alpha-T) and the chemo drug, Doxorubicin (Doxo, as a positive control). Cell viability assay showed that T(3) significantly (P < or = 0.05) lowered the percentage of BNL 1ME A.7R.1 cell viability in a dose-responsive manner (8-16 microg mL(-1)), whereas T did not show any significant (P>0.05) inhibition in cell viability with increasing treatment doses of 0-16 microg mL(-1). The IC(50) for tocotrienols were 9.8, 8.9, 8.1, 9.7, 8.1 and 9.3 microg mL(-1) at 12, 24, 36, 48, 60 and 72 hours respectively. Early apoptosis was detected 6 hours following T(3) treatment of BNL 1ME A.7R.1 liver cancer cells, using Annexin V-FITC fluorescence microscopy assay for apoptosis, but none were observed for the non-treated liver cancer cells at the average IC(50) of 8.98 microg mL(-1) tocotrienols for liver cancer cells. Several apoptotic bodies were detected in BNL 1ME A.7R.1 liver cancer cells at 6 hours post-treatment with tocotrienols (8.98 microg mL(-1)) using Acridine Orange/Propidium Iodide fluorescence assay. However, only a couple of apoptotic bodies were seen in the non-treated liver cancer cells and the BNL CL.2 normal liver cells. Some mitotic bodies were also observed in the T(3)-treated BNL 1ME A.7R.1 liver cancer cells but were not seen in the untreated BNL 1ME A.7R.1 cells and the BNL CL.2 liver cells. Following T(3)-treatment (8.98 microg mL(-1)) of the BNL 1ME A.7R.1 liver cancer cells, 24.62%, 25.53% and 44.90% of the cells showed elevated active caspase 3 activity at 9, 12 and 24 hours treatment period, respectively. DNA laddering studies indicated DNA fragmentation occurred in the T(3)-treated liver cancer cells, BNL 1ME A.7R.1 but not in non-treated liver cancer cells and the T(3)-treated and non-treated normal liver cells. These results suggest that tocotrienols were able to reduce the cell viability in the murine liver cancer cells at a dose of 8-32 microg mL(-1) and that this decrease in percentage cell viability may be due to apoptosis.

Animals↗
PubMed1991

Natural killer activity of human liver-derived lymphocytes in various liver diseases.

Liver-derived lymphocytes were isolated from 40 human livers with end-stage liver disease that were removed at the time of orthotopic liver transplantation. In addition, 10 resection specimens or whole livers removed from patients with liver cancer and seven normal livers (unused donor organs) were studied as controls. Liver-derived lymphocytes were isolated from enzymatically digested tissue by gradient centrifugation and adherence to plastic. Their phenotypical characteristics were studied by two-color flow cytometry, and effector cell function was determined in 4-hr 51Cr-release assays against a natural killer-sensitive target, K562 (natural killer activity), natural killer-resistant Daudi line (lymphokine-activated killer activity) and by P815 line with or without phytohemagglutinin to assess lectin-dependent cellular cytotoxicity. Liver-derived lymphocytes isolated from normal liver contained equal proportions of T and natural killer lymphocytes (mean natural killer/T ratio = 0.7). CD3-CD56+CD16- natural killer cells were the main natural killer subset present in liver-derived lymphocytes, in contrast to the predominant natural killer phenotype in the circulation (CD56+CD16+). Control liver-derived lymphocytes had levels of cytotoxicity significantly greater than those of the normal peripheral-blood lymphocytes against all three targets. In contrast, liver-derived lymphocytes isolated from organs with advanced liver disease differed markedly in the natural killer/T cell ratio and levels of liver-derived lymphocyte cytotoxicity. Liver-derived lymphocytes obtained from hepatocellular carcinoma or rejecting allografts treated by immunosuppressive therapy had virtually no cytotoxicity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Metabolism and covalent binding of [14C]toluene by human and rat liver microsomal fractions and liver slices.

The in vitro metabolism of [14C]toluene by liver microsomes and liver slices from male Fischer F344 rats and human subjects has been compared. Rat liver microsomes produced only benzyl alcohol from toluene. Liver microsomes from human subjects metabolized toluene to benzyl alcohol, benzaldehyde, and benzoic acid. Liver microsomes from one human donor also produced p-cresol and o-cresol. The overall rate of toluene metabolism by human liver microsomes was 9-fold greater than by rat liver microsomes. Human liver microsomal metabolism of benzyl alcohol to benzaldehyde required NADPH and was inhibited by carbon monoxide and high pH (pH 10). but was not inhibited by ADP-ribose or sodium azide. These results suggest that cytochrome P-450, rather than alcohol dehydrogenase, was responsible for the metabolism of benzyl alcohol to benzaldehyde. Human and rat liver slices metabolized toluene to hippuric acid and benzoic acid. The overall rate of toluene metabolism by human liver slices was 1.3-fold greater than by rat liver slices. Cresols and cresol conjugates were not detected in human or rat liver slice incubations. Covalent binding of [14C]toluene to human liver microsomes and slices was 21-fold and 4-fold greater than to the comparable rat liver preparations. Covalent binding did not occur in the absence of NADPH, was significantly decreased by coincubation with cysteine, glutathione, or superoxide dismutase, and was unaffected by coincubation with lysine. Protease and ribonuclease digestion decreased the amount of toluene covalently bound to human liver microsomes by 78% and 27% respectively. Acid washing of human liver microsomes had no effect on covalent binding.(ABSTRACT TRUNCATED AT 250 WORDS)

Alcohol Drinking↗
PubMed1988

Hormonal control of glycogenolysis in parenchymal liver cells by Kupffer and endothelial liver cells.

Conditioned media of isolated Kupffer and endothelial liver cells were added to incubations of parenchymal liver cells, in order to test whether secretory products of Kupffer and endothelial liver cells could influence parenchymal liver cell metabolism. With Kupffer cell medium an average stimulation of glucose production by parenchymal liver cells of 140% was obtained, while endothelial liver cell medium stimulated with an average of 127%. The separation of the secretory products of Kupffer and endothelial liver cells in a low and a high molecular weight fraction indicated that the active factor(s) had a low molecular weight. Media, obtained from aspirin-pretreated Kupffer and endothelial liver cells, had no effect on the glucose production by parenchymal liver cells. Because aspirin blocks prostaglandin synthesis, it was tested if prostaglandins could be responsible for the effect of media on parenchymal liver cells. It was found that prostaglandin (PG) E1, E2, and D2 all stimulated the glucose production by parenchymal liver cells, PGD2 being the most potent. Kupffer and endothelial liver cell media as well as prostaglandins E1, E2, and D2 stimulated the activity of phosphorylase, the regulatory enzyme in glycogenolysis. The data indicate that prostaglandins, present in media from Kupffer and endothelial liver cells, may stimulate glycogenolysis in parenchymal liver cells. This implies that products of Kupffer and endothelial liver cells may play a role in the regulation of glucose homeostasis by the liver.

Alprostadil↗
PubMed1994

Immunohistochemical phenotyping of liver macrophages in normal and diseased human liver.

The phenotypical heterogeneity of human liver macrophages was analyzed with monoclonal antibodies that recognize antigens specific for the monocyte-macrophage lineage. Most liver macrophages in normal and diseased liver were positive for CD68, whereas fewer matured macrophages were detected by 25-F9. Comparative staining of mirror sections revealed some to be doubly positive and others to be singly CD68 positive. Quantitative analysis confirmed the difference, suggesting heterogeneity of maturation in liver macrophages. Most liver macrophages in the normal liver were negative for CD14, a receptor for lipopolysaccharide and lipopolysaccharide-binding protein complexes. Liver macrophages in liver diseases were activated to express CD14 at varying degrees and were involved in the clearance of lipopolysaccharide-lipopolysaccharide-binding protein complexes. Fc gamma RI, a receptor for monomeric IgG that is involved in antibody-mediated cell cytotoxicity, was negative in the normal liver, but was expressed in liver macrophages at inflammatory sites (e.g., in piecemeal and focal necrosis) in diseased livers. Fc gamma RII was expressed in most liver macrophages, as well as in sinusoidal endothelial cells; Fc gamma RIII was expressed in a smaller number of liver macrophages. Expression of Fc gamma RII and Fc gamma RIII was increased in chronic active hepatitis. These results suggest that liver macrophages are heterogeneous in maturation and function and that they are activated in liver diseases as shown by the novel expression of CD14 and Fc gamma RI. The restricted expression of Fc gamma RI indicates that Fc gamma RI-positive macrophages, in cooperation with cytotoxic T lymphocytes, may play an important role in liver cell injury through antibody-mediated cell cytotoxicity.

Antigens, CD↗
PubMed1995

Coexpression of liver-specific and growth-induced genes in perinatal and regenerating liver: attainment and maintenance of the differentiated state during rapid proliferation.

The liver shows maximal cellular growth during fetal development and after partial hepatectomy. Exploring overlaps in gene expression patterns in these two types of hepatic growth may provide insight into common regulatory pathways. The expression of a large number of growth-induced and liver-specific genes induced in liver regeneration has been examined in the perinatal liver from several days prenatal to 4 weeks postnatal when the major growth phase of the liver ceases. As in liver regeneration, many growth-induced genes, such as PRL-1 and beta-actin, are expressed at a high level throughout the temporal course of liver development and correlate with the proliferative state. The level of fetal liver expression of these genes is similar to peak expression found in the regenerating liver, suggesting that common pathways of transcriptional regulation exist in the two types of proliferation. A subset of liver-restricted immediate-early genes including, IGFBP-1, CL-6, and glucose-6-phosphatase (G6Pase) are induced in regenerating liver and may be important in maintaining hepatic metabolism during regeneration. In developing liver, these genes are expressed primarily in the perinatal period but, unlike the regenerating liver, are not coinduced. For instance, at birth, G6Pase is induced, whereas CL-6 is downregulated. In situ analyses confirm that a proliferation associated gene PRL-1 is expressed in multiple cell types throughout the developing liver, whereas the expression of liver-specific genes is confined to hepatocytes. Taken together, these findings imply that significant similarities and differences in transcriptional regulation and hormonal milieu exist in liver during regeneration and development.(ABSTRACT TRUNCATED AT 250 WORDS)

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