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T Berg

Publications and source records attributed to T Berg.

At least 109 records · Page 6Linked to original sources
PubMed1998

A clinical and virological study of hepatitis C virus-related cryoglobulinemia in Germany.

BACKGROUND/AIMS: Several reports, especially from Southern Europe, have demonstrated a close association between hepatitis C virus (HCV) infection and mixed cryoglobulinemia. In this study we have analyzed the significance of HCV-related cryoglobulinemia in Germany. METHODS: Sera from 79 patients with cryoglobulinemia of type I (n=21), II (n=28) or III (n=30) were investigated for HCV markers. Furthermore, 132 consecutive patients with chronic hepatitis C were studied for the presence of cryoglobulins. Genotypes of HCV were determined according to Simmonds, and HCV-RNA concentrations were measured in patients with and without cryoglobulinemia. RESULTS: In 79 patients with cryoglobulinemia we found anti-HCV antibodies in 17 (22%) and HCV-RNA in 11 patients (14%). HCV antibodies were more frequent in essential (44%) compared to secondary mixed cryoglobulinemia (15%). In 132 patients with chronic HCV infection cryoglobulins were detected in 37 patients (28%), in 21 of them at low levels. Clinical symptoms due to cryoglobulinemia were observed in eight of the 37 patients, severe vasculitis in three patients with high cryocrit-levels and cryoprecipitation at room temperature. HCV genotype 1 and subtype 1b were most prevalent, both in patients with and without cryoglobulinemia, and mean HCV-RNA levels were not different between the two groups. Comparison of HCV-RNA levels in cryoprecipitates, supernatant and native serum suggests binding of HCV-RNA to the cryoprecipitate with different affinity in individual patients. CONCLUSIONS: The lower prevalence of HCV-related cryoglobulinemia in our study compared with data from Italy and France suggests a south-north gradient in the prevalence of HCV-associated cryoglobulinemia in Europe.

Adult↗
PubMed1998

Quality control study on the performance of GB virus C/hepatitis G virus PCR.

BACKGROUND/AIMS: A novel virus, GBV-C/HGV, with a genome RNA organization similar to that of the Flaviviridae family was identified in sera of patients with hepatitis. The presence of GBV-C/HGV RNA can only be determined by the amplification of genomic regions using the reverse transcriptase-polymerase chain reaction (RT-PCR). METHODS: To assess the quality of the RT-PCR, 14 laboratories investigated a coded serum panel that comprised three GBV-C/HGV RNA-positive sera from three different patients, dilutions of these sera, and three GBV-C/HGV RNA-negative serum samples, two of which were collected from patients with hepatitis C but without GBV-C/HGV infection. In-house RT-PCR as well as commercially available GBV-C/HGV test kits were used in this study. RESULTS: Only four laboratories (29%) reported the expected results, and four laboratories (29%) false-positive results; nine laboratories (64%) reported at least one false-negative result. Eleven laboratories (79%) detected the undiluted samples. The majority of false results were obtained with the dilutions of GBV-C/HGV RNA-positive samples. Negative results in the 10(-4) dilution were not considered to be false-negative, since during pre-screening GBV-C/HGV RNA had been detected in this dilution in only 50% of assays by the three laboratories involved in organizing the evaluation. Results obtained by commercial kits and by in-house assays were indiscriminate in quality of performance in this study. CONCLUSION: To facilitate further quality assessment studies on the performance of GBV-C/HGV RNA detection, an international GBV-C/HGV RNA standard should be made available. Further efforts are required to optimize GBV-C/HGV RT-PCR.

Austria↗
PubMed1998

Expression of retinoic acid receptor and retinoid X receptor subtypes in rat liver cells: implications for retinoid signalling in parenchymal, endothelial, Kupffer and stellate cells.

In the present study, a systematic examination of the relative expression pattern of the nuclear retinoid receptors (RAR and RXR) in various liver cells was performed. Our data demonstrate that RXRalpha is the dominant receptor in all liver cells, and that RARbeta is also expressed at a high level in most cells. More specifically, RARbeta and RARalpha were the most predominant of the RAR subtypes in parenchymal cells, while all three RAR subtypes were equally expressed in endothelial and Kupffer cells. The total level of expression of all the RXR subtypes were larger than the total level of expression of all the RAR subtypes in all liver cells. This is in agreement with the observation that RXR is a heterodimer partner not only for RAR, but also for other members in the steroid/thyroid receptor superfamily of ligand-dependent transcription factors.

Animals↗
PubMed1998

Persistent hepatitis G virus infection after neonatal transfusion.

BACKGROUND: Recently two Flaviviridae-like viruses have been discovered and named GB virus C and hepatitis G virus. Molecular characterization showed them to be different subtypes of the same virus. An association with posttransfusion hepatitis and with sporadic and fulminant hepatitis was reported, but most infected people remain asymptomatic. Data concerning hepatitis G virus infection in infants and children have not been reported to date. The prevalence of hepatitis G virus infection in children after transfusion of blood products in the neonatal period was studied. METHODS: Serum samples from 251 children, who had received blood products in the first 4 weeks of life and who had been reexamined as part of another study at a mean interval of 37 months (range, 10-70) after last transfusion, were analyzed for hepatitis G virus infection. Follow-up examinations were performed in 14 of 19 hepatitis G virus-positive children 12 to 17 years after the last transfusion. Presence of hepatitis G virus RNA in serum was determined by a reverse transcription polymerase chain reaction assay with nested primers from the helicase region of the hepatitis G virus. To prove specificity of the hepatitis G virus, reverse transcription polymerase chain reaction assay and compare follow-ups with initial sequences, direct sequencing of the NS3 and NS5 regions of the hepatitis G virus was performed. RESULTS: Hepatitis G virus RNA was detected in 19 of 251 patients (7.6%); sequence analysis showed the isolates to be of hepatitis G virus type. None of the patients with hepatitis G virus infection had evidence of liver disease, although 3 patients were coinfected with hepatitis C virus. Four of 14 patients who were reinvestigated after a mean of 15 years showed persistent hepatitis G virus infection. Each of the 4 children was healthy. In none were clinical signs of liver disease observed; liver function test results were within the normal range. CONCLUSIONS: Children receiving blood transfusions in the neonatal period are at increased risk of hepatitis G virus infection with a high rate of chronic infection. However, as in the findings in several studies of adult transfusion recipients, in the current results, no association between hepatitis G virus infection and clinical or biochemical signs of hepatitis or extrahepatic disease could be seen.

Base Sequence↗
PubMed1998

Detection of sequences of TT virus, a novel DNA virus, in German patients.

Recently a novel DNA virus, designated TT virus (TTV), that possibly accounts for some of the cases of liver disease of unknown aetiology, was identified in Japanese patients. Using specific primer pairs for conserved regions, we detected TTV DNA by PCR in 16/84 (19%) German patients awaiting orthotopic liver transplantation because of decompensated liver cirrhosis (of diverse causes); in 4/25 (16%) patients with non-A-G hepatitis; in 1/7 patients with autoimmune hepatitis; and in one intravenous drug user. Sequence analysis showed that in contrast to the findings in Japanese patients only about 37% of our TTV sequences belonged to genomic group 1 but about 58% belonged to group 2, including several sequences belonging to a further subgroup tentatively designated group 2c. Further studies to clarify whether the novel virus has hepatitis-inducing capacity or other clinical significance are needed.

Amino Acid Sequence↗
PubMed1998

Complete nucleotide sequence of pSK41: evolution of staphylococcal conjugative multiresistance plasmids.

The 46.4-kb nucleotide sequence of pSK41, a prototypical multiresistance plasmid from Staphylococcus aureus, has been determined, representing the first completely sequenced conjugative plasmid from a gram-positive organism. Analysis of the sequence has enabled the identification of the probable replication, maintenance, and transfer functions of the plasmid and has provided insights into the evolution of a clinically significant group of plasmids. The basis of deletions commonly associated with pSK41 family plasmids has been investigated, as has the observed insertion site specificity of Tn552-like beta-lactamase transposons within them. Several of the resistance determinants carried by pSK41-like plasmids were found to be located on up to four smaller cointegrated plasmids. pSK41 and related plasmids appear to represent a consolidation of antimicrobial resistance functions, collected by a preexisting conjugative plasmid via transposon insertion and IS257-mediated cointegrative capture of other plasmids.

Amino Acid Sequence↗
PubMed1998

Degradation of phagosomal components in late endocytic organelles.

Phagosomes are formed when phagocytic cells ingest particles such as bacteria, viruses or synthetic beads of different kinds. The environment within the phagosome gradually changes to generate degradative conditions. These changes require multiple interactions between the maturing phagosomes and the endocytic and the biosynthetic pathway. The phagosomes probably communicate with endocytic organelles by a transient fusion event, often referred to as the 'kiss-and-run' hypothesis. We have studied the role of endocytic organelles in the phagocytic pathway of J774 cells, a mouse macrophage cell line. We have used magnetic Dynabeads coated with 125ITC-IgG and 125ITC-OVA as phagocytic probes and were able to isolate the phagosomal fraction by means of a magnet. To separate lysosomes from other organelles in the endocytic pathway we allowed the cells to endocytose a pulse of colloidal gold particles complexed with ovalbumin. By combining this density shift technique with subcellular fractionation of a postnuclear supernatant in Percoll gradients we could isolate three endocytic fractions corresponding to early endosomes (the light Percoll fraction), late endosomes (the dense Percoll fraction) and lysosomes (the gold fraction). We observed that the proteins linked to the ingested beads are initially cleaved in the phagosomes. This cleavage is inhibited by leupeptin, a thiol-protease inhibitor, and requires an acidic environment. However, efficient communication between the phagosomes and the endocytic pathway leads to the transfer of dissociated phagocytosed peptides of different sizes to late endosomes and lysosomes for further processing. Consequently, the late endosomes and the lysosomes may be involved in the degradation of phagocytosed compounds.

Acids↗
PubMed1998

Epidemiological and clinical aspects of hepatitis G virus infection in blood donors and immunocompromised recipients of HGV-contaminated blood.

BACKGROUND AND OBJECTIVES: The infectiousness and clinical relevance of the newly discovered blood-borne Flaviviridae-like agent, termed hepatitis G virus (HGV), are not well understood. MATERIALS AND METHODS: Twenty-three transfusion recipients of two HGV-affected long-term blood donors were studied for HGV genome and antibodies to the putative envelope 2 glycoprotein (anti-E2) of HGV. Nine recipients had nonhematological disorders and 14 suffered from severe hematological diseases and 7 of them received allogeneic bone marrow or blood stem cell transplantation. The molecular epidemiology of the observed HGV infection was studied by direct sequencing of parts of the 5'-noncoding region, NS3, and NS5 region of HGV in the 2 long-term donors and in their 6 recipients who became HGV RNA positive. Additionally, 549 individuals-homologous (n = 254) and autologous blood donors (n = 202), and medical staff (n = 89)--were investigated for the presence of HGV RNA. RESULTS: HGV RNA in serum was found in 15 of the 23 (65%) transfusion recipients with known exposure of HGV-contaminated blood. Seven of the remaining 8 recipients showed only an anti-E2 response, indicating previous HGV infection with spontaneous clearance of the virus. In one recipient neither HGV RNA nor anti-E2 could be detected. Molecular evidence for HGV transmission by the 2 donors was found in 3 of the 6 recipients studied. The alanine aminotransferase levels were not significantly different in the HGV RNA positive and negative recipients, and none of the 23 recipients developed posttransfusion hepatitis. Persistent HGV infection was observed especially in recipients with severe hematological disorders or in those in whom intensive immunosuppressive treatment was necessary. Of the 549 individuals studied, 10 (1.8%) were healthy carriers of HGV RNA. CONCLUSION: The persistence of transfusion-acquired HGV infection is not associated with acute or chronic hepatitis, but may be influenced by the recipient's underlying disease.

Adult↗
PubMed1997

Recent trends in atmospheric deposition of trace elements in Norway as evident from the 1995 moss survey.

Atmospheric trace element deposition in Norway has been evaluated by using data from a national moss survey from 1995, comprising 53 elements in 458 samples of the ground growing moss Hylocomium splendens. The results are compared with similar surveys carried out in 1977, 1985 and 1990 in order to evaluate temporal deposition trends. Atmospheric long-range transport (LRTP) from other parts of Europe is the main source for deposition of V, Zn, As, Mo, Ag, Cd, Sn, Sb, Hg, Tl, Pb and Bi in Norway. Between 1977 and 1990 the levels of most of the LRTP elements monitored (V, Zn, As, Cd, Sb, Pb) were reduced by more than 50%. Between 1990 and 1995, no further decrease has been observed for any of the LRTP elements, except for Pb where a further reduction is evident. The most north-easterly part of Norway is exposed to high levels of Co, Ni and Cu from emission sources from the Kola peninsula, Russia and the levels have not changed significantly since 1977. A new ferro-chrome smelter at Mo i Rana, northern Norway has resulted in a substantially enhanced deposition of Cr in the surrounding area.

Air Pollution↗
PubMed1997

Purification of feline lysosomal alpha-mannosidase, determination of its cDNA sequence and identification of a mutation causing alpha-mannosidosis in Persian cats.

alpha-Mannosidosis is a lysosomal storage disorder that is caused by the deficiency of lysosomal alpha-mannosidase. Feline alpha-mannosidosis is a well-characterized animal model used for studying pathological and therapeutic aspects of lysosomal storage disorders. We here report the purification of feline liver lysosomal alpha-mannosidase and determination of its cDNA sequence. The active enzyme consisted of three polypeptides, with molecular masses of 72, 41 and 12 kDa, joined by non-covalent forces. The cDNA sequence of feline lysosomal alpha-mannosidase was determined from reverse transcriptase PCR products obtained from skin fibroblast mRNA. The deduced amino acid sequence contained the N-terminal sequences of the 72 and 41 kDa peptides. This indicated that the enzyme is synthesized as a single-chain precursor with a putative signal peptide of 50 amino acids followed by a polypeptide chain of 957 amino acids, which is cleaved into the three polypeptides of the mature enzyme. The deduced amino acid sequence was 81.1 and 83.2% identical with the human and bovine lysosomal alpha-mannosidases sequences respectively. A 4 bp deletion was identified in an alpha-mannosidosis-affected Persian cat by DNA sequencing of reverse transcriptase PCR products. The deletion resulted in a frame shift from codon 583 and premature termination at codon 645. No lysosomal alpha-mannosidase activity could be detected in the liver of this cat. A domestic long-haired cat expressing a milder alpha-mannosidosis phenotype than the Persian cat had a lysosomal alpha-mannosidase activity of 2% of normal. This domestic long-haired cat did not possess the 4 bp deletion, proving molecular heterogeneity for feline alpha-mannosidosis.

Amino Acid Sequence↗
PubMed1997

Genomic structure of the human lysosomal alpha-mannosidase gene (MANB).

Lysosomal alpha-mannosidase (LAMAN) (EC 3.2.1.24) is an exoglycosidase involved in the ordered degradation of N-linked oligosaccharides. Lack of LAMAN activity leads to the lysosomal storage disorder alpha-mannosidosis (MIM No. 248500). We determined the genomic organization of the human lysosomal alpha-mannosidase gene (laman; HGMW-approved symbol MANB) by using oligonucleotide primers designed from the human laman cDNA sequence as part of a PCR-based strategy. The gene spanned 21.5 kb and contained 24 exons. By primer extension analysis, the major transcription initiation sites were mapped to positions -309, -196, and -191 relative to the first in-frame ATG. No CAAT or TATA sequences could be identified within 134 bp upstream of the transcription initiation sites, but the 5' flanking region contained several GC-rich regions with putative binding sites for the transcription factors SP-1, AP-2, and ETF.

Base Sequence↗
PubMed1997

Purification of bovine lysosomal alpha-mannosidase, characterization of its gene and determination of two mutations that cause alpha-mannosidosis.

Bovine kidney lysosomal alpha-mannosidase was purified to homogeneity and the gene was cloned. The gene was organized in 24 exons that spanned 16 kb and its corresponding cDNA contained an open reading frame of 2997 bp beginning from a putative ATG start codon. The deduced amino acid sequence contained a signal peptide of 50 amino acids adjacent to a protein sequence of 949 amino acids that was cleaved into five peptides in the mature enzyme; starting with the peptide derived from the N-terminal part of this precursor, their molecular masses were 35/38 (peptide a), 11/13 (peptide b), 22 (peptide c), 38 (peptide d) and 13/15 kDa (peptide e). Variation in the degree of N-glycosylation accounts for molecular mass heterogeneities of peptides a, b and e. Peptides a, b and c were disulphide-linked. A T961-->C transition, resulting in Phe321-->Leu substitution, was identified in the cDNA of alpha-mannosidosis-affected Angus cattle. In affected Galloway cattle, a G662-->A transition that causes Arg221-->His substitution was identified. Phe321 and Arg221 are conserved among the alpha-mannosidase class-2 family, indicating that the substitutions resulted from disease-causing mutations in these breeds.

Amino Acid Sequence↗
PubMed1997

The expression of endosomal rab proteins correlates with endocytic rate in rat liver cells.

Hepatic endocytosis is characterized by a division of labor between the different cell types with respect to endocytosis, which is mediated by receptors expressed on their cell surface. We have investigated the expression of GTPases of the rab family in rat liver parenchymal and endothelial cells. Small GTPases of the rab protein family control distinct steps of intracellular transport both in the secretory and the endocytic pathway. As controls have been employed the normal rat kidney (NRK) cell line and brain tissue, neuronal cells are known to express high levels of components of the endocytic machinery (clathrin, adaptins, dynamin, uncoating adenosine triphosphatase, etc.). Endothelial cells were found to express four to seven times more rab4, rab5, and rab7 than parenchymal cells. A similar relationship was found between the endocytic rates in the two cell types; the rate of internalization from the plasma membrane of mannose receptors in rat liver endothelial cells was 2.3 pools/min, whereas the corresponding value for internalization of the galactose receptor in parenchymal liver cell was 0.27 pools/min (comparable with the rate of transferrin internalization in NRK cells). Both immunofluorescence and subcellular fractionation experiments showed that rab5 and rab7 were associated with compartments along the endocytic pathway. Brain tissue showed a similar high expression of endocytic components (rab4, rab5, and rab7) as liver endothelial cells, whereas lower values were found in NRK cells. We also analyzed the following proteins involved in endocytosis: clathrin, alpha-adaptin, beta-adaptin, and rabaptin-5. These proteins showed the same pattern of expression as the rab proteins. In conclusion, the results obtained with liver cells corroborate the data obtained in transfected cells and support the notion that rab proteins may be involved in controlling the endocytic rate in liver cells.

Animals↗
PubMed1997

A pretransplant infection with precore mutants of hepatitis B virus does not influence the outcome of orthotopic liver transplantation in patients on high dose anti-hepatitis B virus surface antigen immunoprophylaxis.

Hepatitis B virus (HBV) infection of the liver graft is a major complication after orthotopic liver transplantation (OLT) for HBV-related cirrhosis. A high viral load before OLT is a known risk factor, whereas the relevance of precore mutants of HBV is a subject of controversy. The aim of this study was to correlate the pretransplantation viral load and a pretransplantation infection with precore mutant HBV (pmHBV) or wildtype HBV (wtHBV) with allograft damage, graft failure, and survival after OLT. Sixty-nine patients with HBV cirrhosis underwent OLT under high dose immunoprophylaxis with anti-hepatitis B surface (HBs) hyperimmunoglobulins (HBIg). A pretransplantation infection with pmHBV and wtHBV was detected by polymerase chain reaction (PCR) and direct sequencing in 30 patients each (pmHBV and wtHBV group). Nine of 69 patients were PCR-negative (noHBV group). Median pretransplantation levels of HBV DNA assessed by hybridization assay were 42 pg/mL for pmHBV and 54 pg/mL for wtHBV patients. HBV recurred in 17 of 30 (57%) of pmHBV and in 14 of 30 (47%) of wtHBV patients and graft failure occurred in 6 of 30 (20%) of pmHBV and 7 of 30 (23%) of wtHBV patients. Neither HBV recurrence nor graft failure occurred in patients in whom no HBV DNA could be detected by PCR using primers flanking the HBV precore region (noHBV) patients. Allograft damage assessed by histology activity index (HAI) scoring was median 6 for pmHBV and 7 for wtHBV patients. Cumulative survival after 5 years was 72% for pmHBV, 74% for wtHBV, and 100% for noHBV patients. In this study, we provide evidence that pretransplantation viral load, but not infection with pmHBV, determines the outcome after OLT in patients on high dose HBIg prophylaxis.

Adult↗