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Biomedical subjects

W Reinhard

Publications and source records attributed to W Reinhard.

13 recordsLinked to original sources
PubMed2001

[Brain central regions in courtship sound production in Drosophila melanogaster].

There are debates about the function of the two main central brain structures of insects--mushroom bodies and the central complex--in the control of motor co-ordination and triggering of different behaviour programs including sound production. To throw additional light onto this problem we analysed the parameters of the love song produced by 5-day old males courting for 5 minutes a fertilised CS female at 25 degrees C, in two wild-type strains of Drosophila melanogaster (Berlin and CS), hydroxyurea (HU)-treated flies (chemical ablation of the mushroom bodies) two mushroom body mutants (mbm1 and mud1), two central complex mutants (ccbKS127 and cexKS181) and a mutant cxbN71 with defects both in the mushroom bodies and in the central complex. It was found that the love song of HU-treated flies devoid of the mushroom bodies is very similar to that of wild-type flies. In mbm1 and mud1 the main parameters of the song (interpulse interval, IPI, and train duration) are slightly shifted from those of wild type but the sharpness of tuning of the pulse oscillator is the same. The flies of all these strains are equal to wild-type strains in mating success (% of copulations with virgins in 10-min test). On the contrary, the songs of the central complex mutants differ from those of wild-type flies. First of all, the sharpness of tuning of the pulse oscillator is destroyed,--the IPIs become highly variable. The pulses often are much longer and polycyclic as in well known cacophony mutant. The mean duration of pulse trains is much shorter. The males of the mutant cexKS181 usually court violently, but in most cases abnormal sounds are produced. Both cexKS181 and ccbKS127 males are much less successful in matings in comparison to wild-type flies. One can conclude that the central complex plays probably a very important role in the control of singing, whereas the mushroom bodies are practically not involved in this function.

Animals↗
PubMed2000

The tumour suppressor protein p53 can repress transcription of cyclin B.

The tumour suppressor protein p53 has functions in controlling the G(1)/S and G(2)/M transitions. Central regulators for progression from G(2) to mitosis are B-type cyclins complexed with cdc2 kinase. In mammals two cyclin B proteins are found, cyclin B1 and B2. We show that upon treatment of HepG2 cells with 5-fluorouracil or methotrexate, p53 levels increase while concentrations of cyclin B2 mRNA, measured by RT-PCR with the LightCycler system, are reduced. In DLD-1 colorectal adenocarcinoma cells (DLD-1-tet-off-p53) cyclin B1 and B2 mRNA levels drop after expression of wild-type p53 but not after induction of a DNA binding-deficient mutant of p53. Analysis of the cyclin B2 promoter reveals specific repression of this gene by p53. Transfection of wild-type p53 into SaOS-2 cells shuts off transcription from a cyclin B2 promoter-luciferase construct whereas a p53 mutant protein does not. The cyclin B2 promoter does not contain a consensus p53 binding site. Most of the p53-dependent transcriptional responsiveness resides in its 226 bp core promoter. Taken together with earlier observations on p53-dependent transcription of cyclin B1, our results suggest that one way of regulating G(2) arrest may be a reduction in cyclin B levels through p53-dependent transcriptional repression.

Cyclin B↗
PubMed1981

[The placebo problem].

Holding placebo response to be a result of magical happenstance and doctor-patient relationship appears less than satisfying. The important factor of spontaneous development in illness, as "visually" demonstrated by Siemens in 1939, is pointed out. The controlled trial is considered analogous to this method. The conditions for carrying out a controlled trial and the control substances are discussed, the deciding criteria for carrying out a placebo-controlled trial are mentioned. The analysis of a placebo-controlled trial is not detrimental to the patient.

Clinical Trials as Topic↗