[Sterilization centers in pharmaceutical field and their developmental trends].
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Biomedical subjects
Publications and source records attributed to A Daniel.
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Constitutive fragile sites (c-fra) comprise the more prevalent but less recognised suite of fragile sites in eukaryotes. They differ from the heritable (rare) suite of fragile sites (h-fra) in several significant ways. In the present report, data concerning the c-fra so far recognised are reviewed in connection with their origin, classification, use as positive controls for cell culture conditions inducing the fra(X), and their presumptive relationships to the characteristic breakpoints in the neoplasias and in constitutional chromosome rearrangements.
The Date of the European Cooperative Prenatal Diagnosis Laboratories (Boué and Gallano, 1984) of 596 prenatal (amniocyte) diagnoses of familial rcp was examined as to relationships between balanced/unbalanced result and ascertainment, carrier parent and chromosome imbalance size (percentage haploid autosome length). Each rearrangement was graphed once with actual (unbalanced result) or potential (normal or balanced result) imbalances plotted with trisomy as the ordinate and monosomy as the abscissa. The graphed data was divided into 15 regions, each of 2.0 per cent trisomy and 0.75 per cent monosomy and the rate of unbalanced pregnancies determined for each region. The highest rates of chromosomally unbalanced progeny (excluding regions with inadequate data) were found closest to the origin (i.e. associated with the smallest imbalances) and these were for ascertainment category 1 (previous rcp unbalanced child) 22.3 per cent for maternal carriers and 39 per cent for paternal carriers. Overall in pooled data for this ascertainment category (without reference to the imbalance graphs) there were for paternal carriers 28.6 per cent unbalanced pregnancies and for maternal carriers 18.1 per cent. The graphed data, therefore, revealed the higher rates associated with some of the rcp with small potential (combined duplication/deficiency) imbalances. Lesser rates were observed for ascertainment category 2 (carrier parent with a history of recurrent miscarriage) with overall percentages of imbalanced progeny ranging from 2.7 (paternal carriers) to 4.7 (maternal carriers). Again, higher rates were revealed in graphed data for small potential imbalances. All unbalanced results for this group (ascertainment category 2) plotted in the region closest to the origin with rates of 16 per cent (maternal carriers) and 9.5 per cent (paternal carriers) in this region. Remarkably in both ascertainment groups 1 and 2 there was no significant difference in the size of the imbalanced segments for unbalanced progeny. In ascertainment group 1 this was (dup/def; mean +/- S.D.): 1.09 +/- 0.77/0.47 +/- 0.45 and in ascertainment group 2: 1.09 +/- 0.80/0.66 +/- 0.71. From the graphed data which arguably denote viability relationships, a trisomy was approximately 2.7 times as likely to survive until amniocentesis as a monosomy of equivalent size. It is proposed that given further data, risk estimates could be determined for rcp heterozygotes using the present approach where empiric data (from the family history or an analysed series of similar rcp) is not available.
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During a 3 weeks period, an immunotherapy by oral route was applied in patients presenting periodontal diseases (gingivitis and chronic adult periodontitis). This study, double blindly conducted, points out a statistically significative decrease of the main clinical symptoms of periodontal diseases (bleeding, erythema, oedema, pain, suppuration, fetidness) without any other local treatment and shows the interest of such a therapy in addition to the classical local treatments applied to patients presenting periodontal diseases.
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