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Biomedical subjects

M Reichert

Publications and source records attributed to M Reichert.

At least 37 records · Page 2Linked to original sources
PubMed2000

Protective effects of a live attenuated bovine leukaemia virus vaccine with deletion in the R3 and G4 genes.

In this study the protective effects of a live attenuated bovine leukaemia provirus (pBLVDX) with deletion in the R3 and G4 genes were tested. Six out of six sheep appeared to resist challenge with parental BLV344. Two out of three animals transfected with pBLVDX were protected against challenge with bovine leukaemia virus (BLV) from a naturally infected cow. As a model for the protection against infection by members of the human T-lymphotropic virus/BLV group, these data provide evidence that a DNA-based vaccination with an attenuated provirus is able to protect against challenge infections.

Animals↗
PubMed2000

[Computer support of workflow in the hospital: concepts, technology and application].

For a variety of reasons, hospitals are developing a growing interest in changing their information systems to support patient processes in a more direct way. This means to actively deliver the tasks to be performed to the right persons at the right point in time with the necessary information and the application functions needed for performing these tasks. Process-oriented workflow technology is a very interesting candidate to achieve this goal. It offers components for the computer-based analysis, modeling, animation, coordination and monitoring of (hospital) processes. In this paper we discuss the perspectives offered by workflow-based, clinical information systems. We survey key features of today's business process modeling tools and of workflow management systems, and we show how they can be applied in the clinical domain. To illustrate the huge potential offered by workflow technology, we present results from the project "Using Workflow Management Systems for Clinical Applications". Within this project we thoroughly analyzed and redesigned core processes from the University's Women hospital and we proto-typically implemented a workflow-based application system for the support of processes from the division day clinic. Although our work shows that current workflow technology is still lacking some important features, in the long run, it may strongly influence information processing within hospitals.

Computers↗
PubMed1999

Analysis of cell cycle arrest in adipocyte differentiation.

Confluent 3T3-L1 preadipocytes differentiate to adipocytes in the presence of insulin, dexamethasone, and isobutylmethylxanthine (IDI). A transient increase of DNA synthesis is induced in 3T3-L1 cells 18 h after addition of IDI, followed by an arrest in the G1 phase of the cell cycle. Growth arrested cells express the proto-oncogene c-myc and the gene for the CCAAT/enhancer binding protein (C/EBPalpha) between day 2 and 5. While c-Myc is strongly implicated in cell proliferation, C/EBPalpha: is a differentiation-specific transcription factor with antiproliferative activity. Here we have characterized the cell cycle arrest in differentiating 3T3-L1 cells. Arrested cells express the Cdk inhibitors p21 and p27, but, at the same time, show hyperphosphorylation of Rb and expression of the E2F-regulated thymidine kinase gene. The addition of new serum to arrested cells resulted in cyclin A expression and Cdk2 activity, but not in DNA synthesis. Simian virus 40 large tumor antigen (LTAg) is a potent mitogen. The mutant LTAg-K1, deficient in binding of pocket proteins and unable to induce DNA synthesis in serum-starved 3T3-L1 cells, efficiently induced DNA synthesis in differentiating 3T3-L1 cells. This indicates that pocket proteins are probably not involved in the control of the cell cycle arrest during 3T3-L1 cell differentiation. Our data suggest that the differentiation-specific cell cycle block in 3T3-L1 cells is resistant to high levels of c-Myc, inactivation of pocket proteins, upregulation of cyclin A levels, and Cdk2 activation, but can be abolished by a function of LTAg that is independent of binding to pocket proteins.

3T3 Cells↗