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R Reichel

Publications and source records attributed to R Reichel.

At least 19 recordsLinked to original sources
PubMed1997

[Carbon-fiber implants for knee ligament reconstruction. 10-year results].

The retrospective results of carbon prostheses for knee ligament reconstruction in 120 patients, as established by questionnaire, are reported at 10 +/- 2 years follow-up. Eighty patients could also be reviewed clinically. Some 60% of the patients showed good subjective function at reduced activity level. Complications were seen in 72.5% of the patients with rupture of the carbon prosthesis and in 68% of those with synovitis. X-ray showed osteoarthritis in up to 59% of the patients. Carbon prostheses for collateral ligament reconstruction (85% medial, 5.8% lateral) were successful in 75% of cases. Activity and time seem to be less responsible for failure of the carbon prostheses than the features of growing in. Destruction of the knee joint over time is due to reactive synovitis and catabolic enzyme reaction and correlates with joint effusion and pain. If these problems appear, (arthroscopic) resection of the synovia is indicated to interrupt the circulus vitiosus.

Adult↗
PubMed1996

Brucella melitensis biotype 1 outbreak in goats in northern KwaZulu-Natal.

Brucella melitensis biotype 1 was confirmed in indigenous, outbred goats in three northern districts of the KwaZulu-Natal province following the diagnosis of human Malta fever in the same area. Six foci of infection were found during an extensive serological survey involving 6266 goats carried out in most of the districts of the KwaZulu-Natal province. The prevalence in the positive herds varied between 17% and 100%. The diagnosis was confirmed by culturing milk samples from serologically positive animals. Infected goats were found in only three districts (Ubombo, Ingwavuma and Pongola) and all infected herds fell within a 50-km radius.

Abortion, Veterinary↗
PubMed1993

E2F site activates transcription in fission yeast Schizosaccharomyces pombe and binds to a 30-kDa transcription factor.

The mammalian transcription factor E2F binds to several cellular proteins including Rb, p107, cyclin A, cyclin E, and p33cdk2 protein kinase in a stage-specific manner during cell cycle. Its recognition sequence, TTTCGCGC, is present in two of the human adenovirus early promoters and in several promoters of cellular genes whose products are implicated in the control of cell proliferation. These observations suggest that E2F may play an important role in cell-cycle regulation and prompted us to ask whether E2F-like activities are present in yeast. We found that the E2F motif can function as an activating sequence in Schizosaccharomyces pombe when cloned upstream of a reporter gene. Consistent with this, the expression of adenovirus E2 promoter in S. pombe was dependent on both E2F motifs of this promoter. A protein, spE2F, that binds to the E2F site was partially purified from S. pombe using DNA-affinity chromatography. The binding specificity of this protein was compared to that of human E2F using a number of mutant E2F sites as competitors. These studies showed that spE2F recognizes a sequence closely related to the E2F site. Ultraviolet cross-linking and Southwestern blot studies indicated that the molecular size of spE2F is 30 kDa. Previous studies have shown that a cis-acting element, ACGCGTNA, also called MluI cell cycle box, or MCB, is critical for the regulated expression of cell cycle related genes both in fission and budding yeast. In S. pombe, the cdc10 gene product binds to this element and controls the cell cycle related genes. Electrophoretic mobility shift assays and molecular size determination studies indicated that spE2F is different from that encoded by cdc10. Thus, our studies suggest that spE2F is a novel transcription factor. We discuss these results in light of recent observations about the periodically expressed genes involved in the cell cycle progression in yeast.

Adenoviruses, Human↗
PubMed1990

[Clomiphene citrate ointment in the local treatment of condylomata acuminata].

The hypothesis underlying local treatment of Condylomata acuminata with clomiphene citrate is based on the assumption that susceptibility to this disease in women depends on the relative amount of oestrogen receptors in the affected, as opposed to the unaffected areas. We postulate blockade of these skin receptors after local application of clomiphene citrate ointment. A pilot study was conducted in 15 patients aged 20-33 with Condylomata acuminata. After only 2 months a complete remission was recorded in 12 patients (= 80%).

Administration, Topical↗
PubMed1989

The adenovirus E4 gene, in addition to the E1A gene, is important for trans-activation of E2 transcription and for E2F activation.

Previous experiments have demonstrated that adenovirus infection of human and mouse cells leads to an E1A-dependent activation of the DNA-binding capacity of a cellular transcription factor termed E2F. E2F binds to two sites in the adenovirus E2 early promoter which have been shown to be critical for E1A-dependent E2 early transcription, and the E2F-binding sites can confer E1A-induced transcription to a heterologous promoter. In addition, under a variety of circumstances, the increase in E2F-binding activity coincides with the activation of E2 transcription. We now find that, in addition to the E1A gene, another early viral gene, the E4 gene, is necessary for the activation of E2F-binding activity. Extracts prepared from human 293 cells, which express the E1A and E1B genes, had low levels of E2F activity, whereas infection of 293 cells with the E1A mutant dl312 increased E2F activity. This increase did not occur when 293 cells were infected with dl366, an E4 deletion mutant, nor was there an increase in E2F activity in HeLa cells infected with either dl366 or dl312; however, a coinfection with the two mutants yielded the normal wild-type increase in E2F. Furthermore, infection of HeLa cells with a high multiplicity of dl312, conditions that allow E4 gene expression in the absence of E1A, did not yield an increase in E2F activity. Thus, it appears that both the E1A gene and the E4 gene are directly involved in E2F activation. Measurements of E2 RNA production in a dl366 infection as compared with a wild-type or dl312 infection demonstrate that the E4 gene is essential for full E2 transcription. Furthermore, transfection assays of the E2 promoter demonstrate that, although E1A alone can trans-activate the E2 promoter, it is not as effective as the combination of E1A and E4 in the induction of the E2 promoter. We therefore conclude that the activation of the E2F factor leading to the activation of E2 transcription requires the combined action of both the E1A 289-amino-acid protein and an E4 product.

Adenoviridae↗
PubMed1988

Activation of a preexisting cellular factor as a basis for adenovirus E1A-mediated transcription control.

Transcription of the set of early adenovirus genes is subject to positive control by the viral E1A gene. For one early viral gene, the E2 gene, this induction involves an increase in a cellular promoter-specific factor termed E2F. We have analyzed the kinetics for this induction and find that E2F is present at only very low levels in extracts of uninfected cells or cells infected for up to 3 hr with adenovirus type 5. The factor increases rapidly at 5 hr and reaches a maximal level at 7-8 hr. The kinetics of induction of the factor are thus coincident with the induction of E2 transcription. The 13S E1A gene product (289-amino acid protein), which is required for the efficient activation of E2 transcription in a productive infection, is also responsible for the activation of E2F, because infection with mutant strain pm975 (13S+, 12S-) induces the factor, whereas no increase of E2F occurs in cells infected by mutant strain dl1500 (13S-, 12S+). Finally, increase in the factor does not involve synthesis of any new protein, because extracts prepared from cells infected with adenovirus type 5 and treated with cycloheximide from 1 hr after infection contain approximately the same level of E2F as extracts from infected but untreated cells. From these results, we conclude that activation of E2F, as a posttranslational event, is responsible for the stimulation of E2 transcription by E1A.

Adenovirus Early Proteins↗
PubMed1988

Transactivation by the adenovirus E1A gene.

The 289aa product of the adenovirus E1A gene mediates the transcriptional activation of the set of early viral genes as well as several cellular genes. The E1A protein is not a DNA binding protein but, rather, acts indirectly to achieve the activation. The process of viral gene activation involves the use of cellular transcription factors, and in at least one case, in vivo assays have demonstrated a stimulation of stable promoter complex formation as a function of the E1A gene product. Analysis of transcription factors in nuclear extracts has identified a cellular factor, termed E2F, with specificity for the viral E2 promoter. The concentration of this factor increases as a result of the action of E1A. This increase in DNA binding activity does not require protein synthesis, thus indicating an E1A-mediated modification of a pre-existing factor. The E2F factor has been purified to homogeneity and is a polypeptide of 54,000 molecular weight. Analysis of an additional viral promoter, the E4 promoter, has identified a protein that interacts with sequences critical for transcription. This factor, termed E4F, is also increased as a function of the E1A product. The E4F factor has also been purified to homogeneity and has a molecular weight of 50,000. Therefore, the coordinate control of transcription by the E1A gene product involves the activation of multiple promoter specific factors.

Adenoviridae↗
PubMed1987

Developmental control of a promoter-specific factor that is also regulated by the E1A gene product.

We have detected a cellular factor in F9 teratocarcinoma cells that recognizes an adenovirus E1A inducible promoter. This factor, termed E2F, was previously identified in HeLa cells and was found at increased levels as a function of the E1A gene product. Upon differentiation of F9 cells with retinoic acid and cAMP, the factor declines to near undetectable levels, consistent with the control of this factor by E1A and the presence of a cellular E1A-like activity in F9 cells but not in differentiated F9 cells. Finally, if the E1A gene is introduced into differentiated cells by an adenovirus infection, there is a large increase in the level of the factor. We suggest that the control of E2F during F9 differentiation is indeed due to an E1A-like activity.

Adenovirus Early Proteins↗
PubMed1987

Promoter interaction of the E1A-inducible factor E2F and its potential role in the formation of a multi-component complex.

The precise binding site in the adenovirus E2 promoter for the E1A-inducible factor E2F was determined. DNase footprinting revealed two distinct regions of protection which spanned sequences from -33 to -49 and from -53 to -71. Chemical modifications of DNA further delineated nucleotides involved in DNA-protein contacts in each binding region. The E2F binding sites are clearly distinct from the binding site for another E2 promoter binding factor, located at -68 to -80, previously described by SivaRaman et al. [(1986) Proc. Natl. Acad. Sci. USA, 83, 5914-5918]. As determined by DNase footprinting using crude nuclear extracts, both factors were present in extracts of Ad5-infected cells and were found to bind simultaneously to their respective sites on the promoter. In contrast, E2F was not evident in extracts of uninfected cells, whereas there was no difference in the -68 to -80 footprint as a function of the extract. Thus, although multiple factors interact with the E2 promoter, only the E2F factor is unique to the infected extract. The implications of the formation of a multi-factor promoter complex as a possible mechanism of transcriptional regulation are discussed.

Adenovirus Early Proteins↗