Biomedical subjects
Publications and source records attributed to J Malicki.
In this paper authors present complex doses of ionizing radiation from brachytherapy and external beam therapy. Doses were determined on Computerized Planning System--Target 2 plus for patients with cancer of cervix.
Mammalian genomes contain clusters of homeobox genes (Hox-C, HOX-C) which are structurally similar to the homeotic genes of the Drosophila HOM complex. One method for assessing the functional similarity of particular Drosophila HOM and mammalian Hox genes is to test the ability of Hox genes to induce homeotic phenotypes when expressed in developing Drosophila. Here we describe such functional tests using mouse HoxB9 (formerly Hox-2.5), whose closest structural relative in Drosophila is Abdominal-B. When expressed from a heat shock promoter, HoxB9 induces transformations of head towards more posterior identities in Drosophila larvae and adults. These transformations share some similarities with the phenotypic effects produced by ectopically expressed Abdominal-B, but are also similar to the transformations induced by Antennapedia and mouse HoxB6 (Hox-2.2), suggesting that HoxB9 specifies a positional identity that is intermediate between Antennapedia and Abdominal-B.
A method of correcting the output dose rate of the radiotherapeutic cobald units is presented. This method links measurements values with the decay formula for increasing the accuracy of output dose rate determining. The least squares method has been applied to mathematical processing of the data. Results were discussed on the record of output dose rate which had been measured since 1969.
Like other homeobox genes of the Antennapedia and bithorax complexes (collectively called the HOM complex), the Drosophila Deformed (Dfd) gene has structural homologues in the Hox/HOX complexes of mouse and humans, one of which is human HOX4B (refs 3, 4). Previous experiments indicated that HOX4B protein can specifically activate the expression of the endogenous Dfd transcription unit in Drosophila embryos and larvae. We therefore asked whether HOX4B cis-regulatory elements could mimic the function of a Dfd autoregulatory element in Drosophila embryos. Here we show that a HOX4B upstream element can surprisingly provide expression in a posterior head segment of Drosophila. One possible mechanism for the axial position-specificity of the human element may involve the conservation of a Dfd-specific autoregulatory circuit in both arthropod and chordate lineages. This possibility is supported by the finding that a Drosophila Dfd autoregulatory element supplies spatially localized expression in the hindbrain of mouse embryos.
Irradiation of cancer diseases with intracavitary applicator makes impossible visual control of applicator's position during the process of irradiation. In this paper example applicator moves during the treatment are presented and their influence to dose distribution especially in reference points is discussed. Verification of applicator's position has been made by the use of roentgen films.
A quick method of calculating the dose-rate distribution in irregularly shaped beams is presented. This method is partly based on the Cunningham model. The proposed modifications make it possible to avoid the scatter functions in favor of direct use of tissue-phantom ratios and field size coefficients. The problem has been evaluated for photons generated by 10 and 23 MV linacs. The calculated dose rates have been compared with measured ones, and good accuracy has been achieved.
The mouse genome has a number of homeobox genes that are structurally similar to the Drosophila Antenapedia (Antp) gene. We find that one of the mouse Antp-like genes, Hox-2.2, when expressed in developing Drosophila cells under control of a heat shock promoter, can induce homeotic transformations that are nearly identical to those caused by ectopic expression of Antp. In larvae, the Hox-2.2-induced transformations include thoracic denticle belts in place of head structures; in adults, the Hox-2.2 transformations include thoracic legs in place of antennae. The phenotypic effects of Hox-2.2 do not depend on the endogenous Antp gene, whose spatial limits of expression are unaffected by Hox-2.2 expression. Thus, in the Drosophila embryo, Hox-2.2 can substitute for some of the segmental identity functions of Antp, presumably by regulating the same set of downstream genes.
We are presenting a method of calculating the dose-rate distributions in partially shielded field. An attenuator was placed in central beam axis and also in an off-axis geometry. The study was made with a Co-60 radiation and with photons generated by 10 and 23 MV Linac at depths, in phantom, from 5 to 30 cm. To obtain the calculated values of dose-rates; the contributions of the three components to the total dose-rate were measured. The calculated dose-rate distributions agree well with the measured data in case of 10 MV and 23 MV radiation.
The bovine papillomavirus (BPV) type 1 E5 gene encodes a 44-amino-acid protein that can stably transform cultured rodent cells when expressed in the absence of all other viral genes. We have previously constructed a BPV-simian virus 40 recombinant virus (Pava-1) which efficiently expresses the BPV type 1 E5 gene in infected cells (J. Settleman and D. DiMaio, Proc. Natl. Acad. Sci. USA 85:9007-9011, 1988). Within 48 h of Pava-1 infection, the vast majority of mouse C127 cells underwent a dramatic morphologic transformation which was accompanied by cell proliferation. Infection of C127 cells made quiescent by contact inhibition and serum starvation caused a great induction of cellular DNA synthesis. These morphologic and mitogenic responses were proportional to the virus multiplicity of infection. Mutational analysis indicated that the E5 gene is both necessary and sufficient for these activities. Analysis of a variety of E5 missense mutants revealed a strong correlation between their phenotypes in the acute transformation assays following infection and in the stable focus-forming assay following transfection. Most of the defective mutants expressed normal levels of E5 protein following infection, indicating that their defective phenotypes are not due to the synthesis of an unstable protein. The failure to genetically resolve these E5 activities suggests that the ability of the E5 protein to cause acute morphologic transformation and reentry into the cell cycle may be intimately related to its ability to cause stable cell transformation and that these functions are probably mediated by a single biochemical activity of the E5 protein.