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Biomedical subjects

E Wendel

Publications and source records attributed to E Wendel.

13 recordsLinked to original sources
PubMed2005

Duration of self assessed benefit of cataract extraction: a long term study.

AIM: To investigate how long patients' improved visual function lasts after a cataract extraction. METHODS: Patients' self assessed visual function was evaluated using the Catquest questionnaire both before and 6 months after a cataract extraction. The study population consisted of 615 patients undergoing a cataract extraction during 1995-2002. A final follow up with a new questionnaire was performed in 2003, between 1 year and 8 years after surgery. RESULTS: 445 (72.4%) patients were alive at follow up and agreed to participate in the study. The number of subjects still showing improved visual function after surgery decreased with longer follow up. After 7 years, 80% had improved visual function compared with before surgery. 50% of all originally operated subjects were alive 7 years postoperatively and enjoyed better visual function than they had done before surgery. Ocular co-morbidity in the operated eye or self assessed poor visual function before surgery was significantly related to deteriorated visual function at follow up. CONCLUSION: The number of subjects who experienced improved visual function after a cataract extraction decreased over the course of time postoperatively. Presence of ocular co-morbidity was significantly related to worsened function.

Aged↗
PubMed1995

c-jun and multistage carcinogenesis: association of overexpression of introduced c-jun with progression toward a neoplastic endpoint in mouse JB6 cells sensitive to tumor promoter-induced transformation.

Tumor promoters such as 12-O-tetradecanoylphorbol-13-acetate (TPA) and epidermal growth factor (EGF) induce neoplastic transformation, elevated c-jun protein expression, and activator protein-1 (AP-1)-dependent gene expression in JB6 mouse epidermal cells sensitive to tumor promoters (clone 415a P+ cells). In contrast, JB6 cells resistant to tumor promoter-induced transformation (clone 307b P- cells) exhibit a greatly reduced TPA or EGF inducible c-jun expression and AP-1 activity. We have recently shown that induced AP-1 is necessary for tumor promoter-induced transformation of P+ cells because introduction of a dominant negative c-jun mutant into P+ cells inhibits both AP-1 dependent transactivation and the transformation response to tumor promoter. The intent of the investigation presented here was to test the hypothesis that elevation of AP-1 activity is sufficient to cause progression to the P+ phenotype in P- cells or to the transformed phenotype in P+ cells. Clonally derived P+ and P- recipient cells transfected with a human c-jun expression construct and overexpressing c-jun protein were tested for progression by assaying for constitutive or inducible anchorage independent phenotype and nude-mouse tumorigenicity. Overexpression of c-jun did not produce progression in P- cells but did increase the probability of progression in P+ cells (two of five transfectant cell lines progressed to the tumor phenotype). In addition, c-jun overexpression did not increase AP-1 activity in any of the P-/c-jun transfectants or in the two of five P+/c-jun transfectants that acquired the transformed phenotype. The P+/c-jun transfectants that showed elevated AP-1 activity did not progress to the tumor phenotype, demonstrating that an increase in AP-1 activity is insufficient for this progression. Since P(+)-to-tumor phenotype progression occurred in cells overexpressing c-jun but not AP-1, we propose that P(+)-to-transformed phenotype progression is c-jun dependent and AP-1 independent.

Animals↗
PubMed1993

Progression toward tumor cell phenotype is enhanced by overexpression of a mutant p53 tumor-suppressor gene isolated from nasopharyngeal carcinoma.

We recently reported the detection of a heterozygous G-->C point mutation at codon 280 of p53 in nasopharyngeal carcinoma, which causes an Arg-->Thr substitution. To test whether this mutant p53 has gained function as an oncogene, we overexpressed the mutant p53 in nontumorigenic cells of two model systems: (i) human Saos-2 cells lacking endogenous p53 and (ii) mouse JB6 variants that bear endogenous wild-type p53. Although they have no growth advantage over the neomycin controls in monolayer culture, human Saos-2 transfectants overexpressing mutant p53 do show enhanced progression to tumor cell phenotype, as assayed by anchorage-independent growth and in vivo tumorigenicity. The enhancement is seen only in transfectants expressing higher levels of p53 protein. In the mouse JB6 system, the mutant p53 functions dominantly in the presence of endogenous wild-type p53 to enhance progression of preneoplastic promotion-sensitive cells toward anchorage-independent phenotype. Mouse JB6 transfectants of mutant p53 are, however, not tumorigenic in nude mice. We conclude from these studies that the G-->C point mutation of p53 at codon 280 is a gain-of-function mutation that appears to operate dominantly and that the mutant p53-thr280 has only moderate oncogenic activity. This mutation may cooperate with other yet-to-be isolated genes in the genesis of nasopharyngeal carcinoma.

Amino Acid Sequence↗
PubMed1982

Responses of preneoplastic epidermal cells to tumor promoters and growth factors: use of promoter-resistant variants for mechanism studies.

The JB6 mouse epidermal cell model system is being used to study the mechanism of promotion of transformation. Promotion of anchorage independence in JB6 cells occurs in response to second-stage but not first-stage promoters, and is inhibited by inhibitors of second-stage not first-stage promotion. A number of variants that are resistant to the phorbol diester TPA have been derived. Some are resistant to plateau density mitogenic stimulation by TPA; others are resistant to promotion of anchorage independence by TPA. Some of the mitogen-resistant variants were promotable by TPA, thus ruling out a requirement for TPA mitogenesis in promotion of transformation in JB6 cells. TPA promotable clones were also sensitive to mezerein and EGF while the TPA nonpromotable variants were also resistant to mezerein and EGF, suggesting that sensitivity to promoters in these JB6 cells is determined at a level distal to receptor binding. Promotion sensitivity did not require available EGF receptors since two TPA promotable variants were EGF receptorless. The mitogenic response of JB6 cells to TPA may however be mediated by EGF since four of four mitogen-resistant variants showed low to zero levels of EGF binding. Tumor promoting phorbol esters produce specific changes in cellular gangliosides. Certain of these changes occur in promotable but not nonpromotable variants of JB6 cells, suggesting that ganglioside changes may be involved in the process of promotion of transformation.

Animals↗
PubMed1979

Ultrastructural studies on the replication of herpes virus ateles-73 in owl monkey kidney cells.

The replicative cycle of herpesvirus ateles, strain 73 (HVA-73), was examined in the electron microscope and compared to that of other herpesviruses known to be oncogenic. A relatively slow replicative cycle of HVA-73 in owl monkey kidney (OMK) cells allowed us to distinguish cytoplasmic and nuclear stages of replication, comprising virus uptake, transport, maturation, and extrusion. Virus uptake was observed within 10 hours of infection and occurred both as a result of fusion between virus and cell membranes and by phagocytosis. Morphologic evidence for the transfer of viral DNA from nuclecapsids to the nucleus at the nuclear membrane is presented. This is shown by the location of numerous empty capsids in front of nuclear pores early during infection. Towards the end of the eclipse phase, at about 48 hougs after infection, two different types of nuclear inclusion bodies were observed. Progeny nucleocapsids were detected in the nucleus at the same time. The envelopment of nucleocapsids occurred both at the nuclear membrane and at proliferating Golgi lamellae in the cytoplasm. Each site of envelopment is associated with the maturation of a characteristic, morphologically distinguishable virus particle. The assembly of HVA-73 resembled that of other oncogenic herpesviruses.

Adsorption↗
PubMed1979

Enhanced proliferation of endogenous virus in Chinese hamster cells associated with microtubules and the mitotic apparatus of the host cell.

Chinese hamster ovary cells harbour intracytoplasmic virus-like particles of type A which are closely associated with sites of microtubule formation. We report here the enhanced proliferation of these particles and their release at the cell membrane by using either 5-bromodeoxyuridine or dibutyryl cyclic AMP. The extracellular mature particles are similar in morphology to retroviruses of type B. Close association of the type A virus precursors with microtubule organizing centres, i.e. kinetochores, centrioles and basal bodies, and with microtubules per se, is confirmed by studying the effects of the microtubule inhibitors Colcemid and vincristine sulphate. The role of microtubules in the activation and transport of the intracytoplasmic type A particles is discussed.

Animals↗