Search PubMed⌕ Search

Biomedical subjects

L Theilmann

Publications and source records attributed to L Theilmann.

At least 145 records · Page 8Linked to original sources
PubMed1985

[Integrated and nonintegrated hepatitis B virus DNA in liver tissue].

Liver tissue was taken in eight patients with virus hepatitis B and one patient with liver carcinoma by biopsy, as well as in seven other patients at post mortem. HBV-DNA was measured in these tissue specimens by hybridization. In four out of eight patients who had had biopsy, HBV-DNA could be found; in two patients it was present in integrated form. The same was true for the tumor tissue stemming from the patient with liver carcinoma. In five out of eight liver tissue specimens taken at post mortem HBV-DNA could be demonstrated as well; it was integrated into the host genom in two cases. It may be important to find out in patients with chronic hepatitis virus infection, if HBV-DNA is present in free or integrated form before antiviral treatment is considered.

Adult↗
PubMed1985

Determination of HBV DNA by a simplified method of spot hybridization.

Molecular hybridization was employed to detect HBV DNA in sera of patients with acute or chronic hepatitis, by a simplified version of the spot hybridization technique. HBV DNA was found in 21 out of 50 sera obtained in acute hepatitis B. Determination of HBV DNA was negative in sera of patients with hepatitis A, Epstein-Bar virus infections or other HBsAg-negative liver diseases. There was no cross-hybridization between HBV DNA and sera of patients with non-A, non-B hepatitis.

Acute Disease↗
PubMed1985

Determination of HBV DNA in serum in a case of needlestick hepatitis.

HBV DNA in serum was determined by modified spot hybridization. A nurse of the dialysis staff was inoculated via needlestick with blood of a HBsAg-positive hemodialysis patient, who had 2000 pg HBV DNA per milliliter serum. After insufficient passive immunization the nurse developed transient anicteric hepatitis B. HBV DNA was positive in sera of the recipient before and at the beginning of the elevation of transaminases.

Adult↗
PubMed1984

[Anti-HBc IgM in acute and chronic hepatitis B virus infection].

Hepatitis B core antigen (HBcAg) synthesized in E. coli was used for determination of immunoglobulin M class-specific antibodies against HBcAg. It was found that 98% of cases with acute hepatitis B surface antigen (HBsAg) positive hepatitis type B were anti-HBc immunoglobulin M (IgM) positive. Atypical hepatitis B was detected in 33% of anti-HBc-positive HBsAg-negative cases with acute hepatitis. Anti-HBc IgM was positive for 6 months in acute resolving hepatitis type B, whereas cases resulting in chronic hepatitis B remained anti-HBc IgM-positive for up to 900 days. Chronic HBsAg carriers with severe liver disease had anti-HBc IgM more often than individuals with minor liver damage; 83% of HBsAg-positive liver cirrhoses, 63% of chronic aggressive hepatitis, 50% of HBsAg-positive liver carcinoma, but only 17% of chronic persistent hepatitis or 7% of healthy blood donors were anti-HBc IgM-positive. Determination of anti-HBc IgM is useful in detecting atypical hepatitis B virus infections without HBsAg in serum and, with some restrictions, in discriminating acute and chronic hepatitis type B.

Acute Disease↗
PubMed1984

Detection of hepatitis B viral DNA in sera positive for antibody to delta antigen.

Hepatitis B virus (HBV) DNA was detected in 17 sera positive for antibody to delta antigen (anti-delta). Six sera from two patients were positive for HBV DNA. Analysis by the Southern blot technique showed identity between HBV DNA in anti-delta-positive and anti-delta-negative sera. These results show that anti-delta-positive sera contain HBV DNA, although these sera were also positive for antibodies to hepatitis B e antigen.

DNA, Viral↗
PubMed1984

HBV-DNA in sera of patients with HBsAg-positive primary liver cell carcinoma.

Sera of ten patients with HBsAg-positive primary liver carcinoma were tested for anti-HBc-IgM and HBV-DNA. Five patients were positive for anti-HBc-IgM and six for HBV-DNA. There was no correlation between the presence of anti-HBc-IgM and HBV-DNA. Our study suggests that complete viral replication exists in some HBsAg-positive primary liver carcinomas.

Aged↗
PubMed1983

Growth-dependent expression of a cell surface glycoprotein.

The expression of the hepatocellular membrane receptor for desialylated galactose-termining glycoproteins was studied during different proliferative stages of a human hepatoma cell line. Rapidly growing cells exhibited a reduced endocytotic rate of desialylated orsomucoid as compared to non-growing cells. This reduction was shown to be the consequence of a lower concentration of active cell-surface associated receptor protein in the dividing cells.

Carcinoma, Hepatocellular↗
PubMed1983

Preparation and metabolism of 125I-sulfobromophthalein.

Metabolism of 125I-sulfobromophthalein (BSP) prepared by the chloramine-T method was studied in rats. 125I-BSP is removed rapidly from the circulation. However, as compared to BSP, its plasma clearance and biliary excretion are delayed, and its accumulation in the liver is prolonged. Although BSP and 125I-BSP show similar binding to albumin in serum, their binding properties to liver cytosolic proteins and to the liver cell plasma membrane organic anion binding protein (OABP) differ. In contrast to the X-, Y- and Z-protein binding of BSP, 125I-BSP binds predominantly to a high molecular weight protein and only a small proportion of 125I-BSP binds to OABP.

Animals↗
PubMed1983

Hepatic bilirubin uptake in the isolated perfused rat liver is not facilitated by albumin binding.

Bilirubin uptake by the liver is a rapid process of high specificity that has kinetic characteristics which suggest carrier-mediation. In the circulation, bilirubin is readily bound to albumin, from which it is extracted by the liver. Although several studies suggested that it is the small, unbound fraction of bilirubin which interacts with hepatocytes and is removed from the circulation, recent experiments have been interpreted as suggesting that binding to albumin facilitates ligand uptake. A liver cell surface receptor for albumin has been postulated. The present study was designed to examine directly whether albumin facilitates the hepatic uptake of bilirubin and whether uptake of bilirubin depends on binding to albumin. Rat liver was perfused with a protein-free fluorocarbon medium, and single-pass uptake of 1, 10, or 200 nmol of [3H]bilirubin was determined after injection as an equimolar complex with 125I-albumin, with 125I-ligandin, or free with only a [14C]sucrose reference. Uptake of 10 nmol of [3H]bilirubin was 67.5 +/- 3.7% of the dose when injected with 125I-albumin, 67.4 +/- 6.5% when injected with 125I-ligandin, and 74.9 +/- 2.4% when injected with [14C]sucrose (P greater than 0.1). At 200 nmol, uptake fell to 46.4 +/- 3.1% (125I-albumin) and 63.3 +/- 3.4% [( 14C]sucrose) of injected [3H]bilirubin (P less than 0.01), which suggests saturation of the uptake mechanism. When influx was quantitated by the model of Goresky, similar results were obtained. When [3H]bilirubin was injected simultaneously with equimolar 125I-albumin and a [14C]sucrose reference, there was no delay in 125I-albumin transit as compared with that of [14C]sucrose. This suggested that the off-rate of albumin from a putative hepatocyte receptor would have to be very rapid, which is unusual for high affinity receptor-ligand interaction. There was no evidence for facilitation of bilirubin uptake by binding to albumin or for interaction of albumin with a liver cell surface receptor. These results suggest that the hepatic bilirubin uptake mechanism is one of high affinity which can extract bilirubin from circulating carriers such as albumin, ligandin, or fluorocarbon.

Animals↗
PubMed1981

[Serum lysozyme activity of serum and umbilical cord blood in newborn babies-diagnostic value of the enzyme in infants with susceptibility to infections and in cases of septicemia. (author's transl)].

Lysozyme levels were determined in serum and umbilical cord blood of 352 newborns and prematures. Levels in premature babies were found to be significantly lower than those of matures at the first day of life. A correlation was seen between the serum lysozyme and the birth weight of 219 mature newborns. In 14 premature babies with clinical signs of sepsis the concentrations of serum lysozyme were particularly decreased in cases of septicemia caused by gram-negative organisms. Serum levels of lysozyme in cord blood were significantly lower in 38 newborns with predisposition to septicemia (above all premature rupture of membranes greater than 24 hr.) comparing with healthy infants. The decreased serum levels of lysozyme in newborns with septicemia and the remarkable susceptibility of infections in male newborns are discussed.

Birth Weight↗
PubMed1980

[Urinary levels of lysozyme in children with acute chronic recurrent urinary tract infection (author's transl)].

Urinary levels of lysozyme activity were measured in 32 children afflicted with acute or chronic urinary tract infection and compared to a group of 30 healthy subjects. A significant difference in the levels of lysozyme activity between the two groups could be observed. In the subjects with acute urinary tract infection the lysozyme levels in the urine were additionally determined at the beginning of the therapy, on the third day, the tenth day and three days after cessation of therapy. High lysozyme levels encountered at the onset of the infection showed under therapy a clear tendency to decrease and in all cases no lysozyme was present three days after therapy was completed. The possible causes of the pathological lysozymuria are discussed. The determination of lysozyme is thus an additional method by which to control the course and outcome of urinary tract infections.

Acute Disease↗
PubMedDate not supplied

Does Z-protein have a role in transport of bilirubin and bromosulfophthalein by isolated perfused rat liver?

Bilirubin and other organic anions are transported in serum avidly bound to albumin from which they are extracted and transferred into the hepatocyte where they bind to cytosolic proteins. Two abundant organic anion binding proteins, ligandin and Z-protein, were previously purified from liver cytosol and characterized. Other studies in isolated perfused rat liver revealed that selectively increased cytosolic ligandin concentration, following phenobarbital treatment or thyroidectomy, directly correlated with net bilirubin uptake which resulted from reduced bilirubin efflux. To clarify the role of Z-protein in hepatic organic anion transport, we have now determined the kinetics of bilirubin and bromosulfophthalein (BSP) uptake in isolated perfused liver of normal rats and compared results to rats in which Z-protein, but not ligandin, was selectively increased following treatment with clofibrate (ethylchlorophenoxy-isobutyrate). These studies revealed that despite a 147% induction of Z-protein in treated animals, there was no effect on influx or efflux of tracer doses of bilirubin or BSP. Addition of albumin to the protein-free 10% fluorocarbon perfusate reduced influx of 3H-bilirubin (p less than 0.03) and tended to reduce influx of BSP. In this situation, there was still no influence of Z-protein concentration on efflux. These studies indicate that Z-protein does not appear to play a role in the hepatic uptake of bilirubin and BSP.

Animals↗
PubMedDate not supplied

Reduced transport of bilirubin and asialoorosomucoid in regenerating rat liver is a microtubule-independent event.

In previous studies, we found that uptake of bilirubin and asialoorosomucoid is depressed in regenerating rat liver. To determine what role the hepatic cytoskeleton plays in this modulation of uptake, animals were treated with colchicine, an inhibitor of microtubular polymerization. Normal unoperated rats or rats following two-thirds hepatectomy or sham surgery were injected with colchicine, lumicolchicine (50 micrograms per 100 gm of body weight, i.p.) or normal saline. Lumicolchicine, an analog of colchicine, has no effect on microtubules and was used as a control. At 12 hr after surgery, sham-operated and unoperated animals received a second equal dose. Partially hepatectomized animals received one-third the initial dose. At 24 hr after surgery, livers were perfused in situ and single-pass multiple indicator dilution studies were performed. Colchicine as compared to lumicolchicine pretreatment reduced apparent influx of bilirubin and asialoorosomucoid in regenerating liver by 50% but had no effect in liver from normal or sham-operated rats. Analysis of indicator dilution curves revealed that reduced influx in colchicine-treated liver was attributable to an increased vascular volume of distribution. These results suggest that microtubules may play a role in maintenance of normal hepatic vascular architecture during regeneration. Lack of effect of colchicine on modulation of bilirubin and asialoorosomucoid uptake during regeneration suggests that other, as yet unknown, factors result in down-regulation of the specific hepatocellular transport systems for these two ligands.

Animals↗
PubMedDate not supplied

Detection of pre-S1 proteins in serum and liver of HBsAg-positive patients: a new marker for hepatitis B virus infection.

The presence of pre-S1 proteins in serum and liver of individuals with acute and chronic hepatitis B virus infection was investigated in Western blots using antibodies against a fusion protein, containing amino acids 20-120 of the pre-S region. Pre-S1 proteins were present in 20 of 38 HBsAg-positive sera. All sera positive for pre-S1 proteins were also positive for hepatitis B virus DNA indicating the presence of hepatitis B virions, and 16 of these sera were also positive for HBeAg. In five sera positive for hepatitis B virus DNA, pre-S1 proteins were not found. In an additional study, pre-S1 proteins could be detected in 4 of 6 patients with acute hepatitis B virus infection during the first 2 weeks after admission to the hospital. The presence of pre-S1 proteins showed a good correlation with the detection of hepatitis B virus DNA. After seroconversion from HBeAg to anti-HBe, both hepatitis B virus DNA and pre-S1 proteins were no longer detectable. Pre-S1 proteins were present in three liver tissue specimens from two patients with acute hepatitis B virus infection and from one patient with cirrhosis of the liver. The proteins were not found in the liver of two HBsAg-positive patients with hepatocellular carcinoma (primary liver carcinoma), negative for HBeAg. Pre-S1 proteins can be detected in serum, positive for hepatitis B virus DNA and in liver tissue of hepatitis B virus-infected individuals. The presence of these proteins appears to correspond with the presence of hepatitis B virus DNA, both markers indicating hepatitis B virus replication.

DNA, Viral↗
PubMedDate not supplied

Expression of apoptosis and apoptosis-related peptides in various stages of rejection in the human transplanted liver.

BACKGROUND/AIMS: In the transplanted liver, the role of apoptosis and apoptosis-related proteins are largely unknown. This study addresses the question whether hepatocyte or leukocyte apoptosis plays an important role in acute rejection of the transplanted human liver and which pathways are involved. METHODOLOGY: Cryosections from liver biopsies with acute rejection were stained with the TUNEL technique for detection of apoptosis and labeled immunohistochemically with antibodies against CD95, bcl-2, TGF-beta and iNOS. A double-labeling protocol was developed for simultaneous detection of iNOS and apoptosis. Liver tissue with chronic viral hepatitis, with hepatitis reinfection and tissue without pathological findings served as a control. RESULTS: Leukocyte apoptosis was markedly reduced in severe compared to mild or moderate acute rejection. Hepatocyte apoptosis is detected rarely in acute rejection with a slight increase from mild to severe despite a strong expression of CD95 and TGF-beta on hepatocytes. The hepatocyte expression of iNOS is weak in acute rejection but strong in control slides with hepatitis B/C reinfection. In acute rejection, simultaneous expression of iNOS and apoptosis could be demonstrated in Kupffer-cells. CONCLUSIONS: Severe acute rejection in the human transplanted liver is characterized by a lack of apoptosis of infiltrating portal lymphocytes probably caused by a reduced downregulation of lymphocyte function. Secondly, in spite of the strong expression of CD95 and TGF-alpha, hepatocyte apoptosis plays a limited role for liver damage in acute rejection. Finally, Kupffer cell apoptosis is increased in acute rejection and seems to be induced by nitric oxide.

Apoptosis↗