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Biomedical subjects

H Greten

Publications and source records attributed to H Greten.

At least 55 records · Page 3Linked to original sources
PubMed1997

Epstein-Barr virus--Associated hemophagocytic syndrome. A cause of fever of unknown origin in human immunodeficiency virus infection.

A 26-year-old human immunodeficiency virus-positive man presented with fever of unknown origin, pancytopenia, and elevated liver function tests. Numerous diagnostic tests and empiric therapeutic interventions remained unsuccessful. Splenectomy eventually established the diagnosis of Epstein-Barr virus-associated hemophagocytic syndrome. Treatment with foscarnet, acyclovir, prednisone, and vinblastine resulted in complete recovery. Three months later, Hodgkin's disease, a previously reported complication of the Epstein-Barr virus-associated hemophagocytic syndrome, was diagnosed. Fever, pancytopenia, and hepatic dysfunction are common complication of advanced human immunodeficiency virus infection and can be caused by a variety of opportunistic pathogens. A high index of suspicion is critical for the management of this otherwise fatal disorder because once the diagnosis is made, even patients with advanced disease benefit from aggressive therapeutic intervention, as demonstrated in the case presented.

Adult↗
PubMed1997

Cellular uptake of lipoprotein[a] by mouse embryonic fibroblasts via the LDL receptor and the LDL receptor-related protein.

The sites and precise mechanisms of the catabolism of the atherogenic lipoprotein[a] (Lp[a]) are unknown. It has been proposed that the low density lipoprotein receptor (LDL-R) and the low density lipoprotein receptor-related protein (LRP) are involved in the catabolism of Lp[a]. To address the question whether and to what extent the LDL-R and/or LRP are involved in the catabolism of Lp[a], we studied the cellular uptake of Lp[a] via those two receptors using mouse embryonic fibroblast (MEF) cell lines lacking either the LDL-R, the LRP, or both receptors due to disruption of the respective mouse genes. 125I-labeled LDL and 125I-labeled Lp[a] uptake by wild-type fibroblasts (MEF1) was compared with that by fibroblasts homozygous for the disrupted LRP allele (MEF2), fibroblasts with two defective alleles for the LDL-R (MEF3), and fibroblasts homozygous for defects both in the LDL-R and LRP gene (MEF4). Compared with MEF1, 125I-labeled LDL uptake by MEF2 was 77%, by MEF3 30%, and by MEF4 24% of that by MEF1. However, no significant differences in the specific 125I-labeled Lp[a] uptake by the four mouse embryonic cell lines was observed. In comparison with MEF1, the 125I-labeled Lp[a] uptake by MEF2 was 98%, by MEF3 111%, and 73% by MEF4. Approximately 50% of the total cellular uptake of 125I-labeled Lp[a] was nonspecific. In conclusion, our results suggest that Lp[a] is a poor ligand for the LDL receptor and the LRP. The data of the displacement studies, however, indicated that the nonspecific uptake of Lp[a] constitutes a major route for the cellular Lp[a] catabolism in this study.

Animals↗
PubMed1997

[Ambulatory sports in asthma improves physical fitness and reduces asthma-induced hospital stay].

Physical training is a well established method in the rehabilitation of patients with chronic obstructive pulmonary disease. In adult asthmatics its efficacy has been shown by intensive training programmes lasting for 2-12 weeks. No data exist on the effect of long-term physical training once a week. 31 patients (f = 24, m = 7; mean age 55 +/- 2 years; mean FEV1.0 82 +/- 4% pred.) participated in a physical training programme for at least 2 years. (8 patients had mild, 12 moderate and 11 severe asthma according to the International Consensus Report of 1993 [13]). Training time was 1 hour per week. The physical training programme consisted of breathing techniques like pursed-lip breathing and diaphragmatic exercise, progressive muscle relaxation, circuits and endurance training. According to the health insurance records 9 patients had been hospitalised for their disease two years prior to the study for a total number of 218 in-hospital days. During the 2 years of the study 2 patients had been hospitalised for a total number of 29 days (p < 0.001). A comparison group of 10 patients who did not participate in the rehabilitation programme had been hospitalised for their disease two years prior to and during the study period for a total number of 236 and 201 in-hospital days (p > 0.2). In a subgroup of 9 patients bicycle exercise testing was performed once a month and work load at a submaximal heart-rate (200-age) was recorded. During the two years mean work rate improved from 48 watts to 83 watts for 15 minutes (p < 0.01). We conclude from our findings that long-term physical training of adult patients with asthma in an outpatient setting once a week is effective in reducing hospitalisation days as well as in increasing cardiorespiratory fitness.

Adult↗
PubMed1996

Hepatitis B virus genomes of patients with fulminant hepatitis do not share a specific mutation.

The pathogenesis of fulminant hepatitis B virus (HBV) infection is not well understood. The aim of this study was to investigate whether there is an association between specific viral variants and a fulminant disease course. The entire HBV genomes from the serum of eight patients with fulminant HBV infection and one patient with fulminant hepatitis during reinfection after liver transplantation were investigated. After isolation and amplification of viral DNA by polymerase chain reaction (PCR), plus and minus strands were directly sequenced. Sequence data were analyzed by comparative sequence alignments with 35 and 2 complete HBV genome sequences from patients without and with fulminant hepatitis, respectively. Several point mutations were present in all regions of the genomes. Many nucleotide changes had never or rarely been found in the reported HBV isolates from patients without fulminant hepatitis. A distinct mutation present in all genomes was not identified. Clusters of rare and unique mutations were observed in the enhancer II core promoter region. Mutations previously suggested to be associated with fulminant HBV infection were not consistently found. A precore stop codon mutation at nucleotide position 1896 or an A-to-T mutation at nucleotide position 1762 and a G-to-A mutation at nucleotide position 1764 in the core promoter region were present in four and three cases, respectively. Fulminant HBV infection does not appear to be caused by a specific genomic mutation. However, various mutations clustering in the enhancer II core promoter region may contribute to a fulminant disease course.

Adult↗
PubMed1996

Differences in the mechanisms of uptake and endocytosis of small and large chylomicron remnants by rat liver.

Initial binding and subsequent endocytosis of small and large chylomicron remnants by rat liver were compared. Small and large chylomicrons were obtained from mesenteric lymph of glucose- or fat-fed rats, respectively. The low-density lipoprotein (LDL) receptor was up- and down-regulated as shown by LDL receptor messenger RNA (mRNA). The rate of removal of small chylomicron remnants by isolated perfused rat livers followed closely the activity of the LDL receptor. When mRNA was undetectable, the uptake was as low as that of lymphatic small chylomicrons. In contrast, the uptake of large chylomicron remnants into perfused rat livers was unaffected by changes of the LDL-receptor activity, but significantly reduced after livers were flushed with heparin or heparinase. Large chylomicron remnants were cleared from plasma much faster than small chylomicron remnants, but were more slowly internalized into hepatocytes. Both, small and large chylomicron remnants entered the pathway of receptor-mediated endocytosis as shown by electron microscopy and analysis of isolated endosomes. Yet, large chylomicron remnants were taken up into the compartment of uncoupling of receptors and ligands and multivesicular bodies at a much slower rate. This was independent of the activity of the LDL receptor and the heparin-releasable binding site. From these findings it is concluded that large chylomicron remnants initially bind rapidly to surface components other than the LDL receptor, one of which may be hepatic lipase. Yet, the consecutive internalization is slow. In contrast, small chylomicron remnants are removed at a slower rate from plasma, binding predominantly to the LDL receptor, but are more readily taken up into endosomes.

Animals↗
PubMed1996

Resolution of HIV-associated cystic benign lymphoepithelial lesion of the parotid gland in a patient undergoing chemotherapy for non-Hodgkin's lymphoma.

Cystic benign lymphoepithelial lesion, a previously rare lesion of the parotid gland characterized by multiple cysts accompanied by marked lymphoid hyperplasia, is increasingly reported in patients with human immunodeficiency virus infection. The case of a 59-year-old man without identifiable risk factors for the acquired immunodeficiency syndrome is presented, in whom the development of cystic benign lymphoepithelial lesions led to the diagnosis of the underlying human immunodeficiency virus infection. The lymphoepithelial lesion remained unchanged for 8 years. When chemotherapy was instituted for abdominal non-Hodgkin's lymphoma all cystic lesions resolved completely. This previously undescribed phenomenon strongly supports the concept that the development of the cysts is secondary to the mechanical obstruction of salivary ducts caused by lymphoid hyperplasia and not due to true de novo cyst formation.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1996

Endocytic mechanisms for uptake and metabolism of chylomicron remnants in the liver.

Removal of small chylomicron remnants by perfused rat livers closely correlates with the LDL-receptor mRNA modulated by various interventions. In contrast, removal of remnants of large chylomicrons is not appreciably influenced by the activity of the hepatic LDL-receptor. Their primary removal depends on a heparinase-sensitive binding site. Transient and stable transfection of the cDNAs of the two subunits of the human asialoglycoprotein receptor markedly increased the binding capacity for chylomicron remnants suggesting the asialoglycoprotein receptor to be an alternative mechanism for remnant removal. Some species can edit apolipoprotein B-100 mRNA and thus secret apolipoprotein B-48 containing lipoproteins of hepatic origin. Generally these animals have lower cholesterol levels and a more favorable lipoprotein profile.

Animals↗
PubMed1996

Rapid plasma virus and CD4+ T-cell turnover in HIV-1 infection: evidence for an only transient interruption by treatment.

OBJECTIVES: To analyse the short-term kinetics of viral plasma RNA and CD4+ T cells numbers in patients with different initial CD4+ T-cell counts treated with different antiretroviral regimens. METHODS: In 10 HIV-1 positive patients, in vivo kinetics of plasma HIV RNA and CD4+ T cells were studied during antiretroviral treatment. Lymphocyte subpopulation analysis, quantitative polymerase chain reaction (PCR), p24 antigen enzyme immunoassay (EIA) and beta 2-microglobulin EIA were performed at days 0, 3, 7, 10, 14, 21 and 28 of treatment. One additional patient served as a control. The resulting curves were fitted. Half-lives were calculated using the time constant T of decrease or increase [T1/2 = In(2) x T]. Calculations of virus and CD4+ T-cell turnover were multiplied by the total blood volume. RESULTS: Viral plasma RNA half-life ranged from 1.1 to 5.1 days, independent of prior or actual treatment and initial CD4+ T-cell count. The calculated peripheral blood viral plasma RNA turnover varied between 0.02 and 55.8 x 10(8) copies/ml/day and showed some negative correlation with initial CD4+ T-cell counts. CD4+ T-cell turnover estimates ranged from 0.01 to 7.5 x 10(8) cells/day. Most patients showed an immediate reincrease of virus load after the nadir. Changes in HIV p24 antigen paralleled HIV plasma RNA in p24 antigen-positive patients. beta 2-microglobulin decreased until day 7-15 in all but one case and rapidly reincreased to pretreatment values. CONCLUSIONS: The kinetics of virus and CD4+ T-cell turnover are uniformly rapid throughout a wide range of initial CD4+ T-cell counts. The magnitude of virus turnover varies considerably among individuals and appears to be inversely related to the initial CD4+ T-cell count. These data also argue for a rapid resumption of virus production and lymphocyte turnover during treatment.

Adult↗
PubMed1996

Transplantation of complete and split liver grafts for patients with fulminant hepatic failure.

Fulminant hepatic failure is associated with considerable mortality under conservative management. The aim of this study was to assess applicability and outcome of liver transplantation using cadaveric and living donated grafts in patients with fulminant hepatic failure. 42 patients presenting with fulminant hepatic failure between 1988 and 1995 were retrospectively analyzed. 37 (88%) met the indication criteria for liver transplantation. 22 patients underwent orthotopic liver transplantation, one patient auxiliary orthotopic liver transplantation. Actual survival rate of these patients is 74% alter a mean follow-up of 23 (3-68) months. 38% (14/37) of the patients with an indication for transplantation did not receive a cadaveric graft due to scarcity of cadaveric organs (n = 9), medical contraindications (n = 3) or spontaneous recuperation (n = 2). Only 21% (3/14) of these patients survived. Due to unavailability of a cadaveric organ four patients, six months to 22 years of age, underwent living related liver transplantation as a last possible treatment option. Three of them died from cerebral herniation. It is concluded that transplantation of a cadaveric graft increased survival rate from 21% to 74% in patients with an indication for liver transplantation. Living related liver transplantation as an individual rescue therapy had no favourable outcome.

Adolescent↗
PubMed1995

Selective uptake of low-density lipoprotein-associated cholesteryl esters by human fibroblasts, human HepG2 hepatoma cells and J774 macrophages in culture.

High-density lipoprotein-(HDL) associated cholesteryl esters (CE) are taken up by hepatic and extrahepatic cells at a higher rate than HDL apolipoproteins. This selective uptake of HDL CE is independent from HDL particle uptake. For low-density lipoprotein (LDL), receptor-mediated endocytosis by cells is well established. In this study, the question was addressed if LDL-associated CE are also taken up by cells independently from LDL particles, i.e., selectively. Human LDL (d = 1.02-1.05 g/ml) was doubly radiolabeled with intracellularly trapped tracers: [125I]Tyramine-Cellobiose ([125I]TC) traced apolipoprotein B, [3H]cholesteryl oleyl ether ([3H]CEt) traced CE. The uptake of doubly radiolabeled LDL by normal and LDL receptor-negative human skin fibroblasts, human HepG2 hepatoma cells and murine J774 macrophages was investigated. Each cell type took up LDL particles as indicated by [125I]TC. However, in fibroblasts, HepG2 cells and J774 macrophages the rate of uptake for LDL-associated [3H]CEt was greater than that according to [125I]TC. These results indicate that extrahepatic and hepatic cells selectively take up LDL CE and this uptake is independent from LDL receptor-mediated endocytosis. Loading cells with cholesterol down-regulated selective uptake of LDL CE. In summary, human skin fibroblasts, human HepG2 cells and murine J774 macrophages selectively take up LDL CE, i.e., CE are taken up independently from LDL particles.

Animals↗