Geometric morphometric methods were used to explore body shape morphology in 260 Atlantic bluefin tuna, Thunnus thynnus, collected in Sardinia (Western Mediterranean) during the breeding phase and in the Bay of Biscay (North Eastern Atlantic) during the feeding phase. The shape of each specimen was captured by high resolution digital images and recording the 2-D coordinates of seven morphological landmarks. A general procruste analysis (GPA) was applied in order to eliminate any morphological variations resulting from size, position or orientation of specimens. A thin plate-spline (TPS) method was then used to provide a graphical representation of the shape conformation between two sets of data. Results of the regression model between the direct and indirect measurements accounted for a R2 = 0.98. The Principal Components Analysis shows differences linked to the two sampling areas, accounting for 37% and 19.97% of the body shape variation in the first (PC1) and second (PC2) principal component, respectively. Specifically, the deformation grid projection highlights the major differences regarding the anterior-ventral part of the body (landmark 5-6-7). These differences might not necessarily be linked to an actual population substructure. Instead, it was hypothesized that such body shape differences were due to the diverse life phases during which specimens were collected, since the reproductive specimens show a 'potbellied' shape, which was larger than for the feeding specimens that showed a 'slimmer' shape. Analyses of likely sexual dimorphism conducted on Sardinian specimens did not reveal any significant differences; whereas body shape differences related to the pre- and post-reproductive sizes were detected
This paper reports our experience of molecular screening and fetal diagnosis of beta-thalassemia in 457 at risk couples of Italian descent. Molecular screening was carried out by dot blot analysis on amplified DNA with oligonucleotide probes complementary to the eight most common mutations in Italians [beta zero 39 (C----T); beta zero 6 (-A); beta+ -87 (C----G); beta+ IVSI nt 110 (G----A); beta zero IVSI nt 1 (G----A); beta+ IVSI nt 6 (T----C); beta zero IVSII nt 1 (G----A); beta+ IVSII nt 745 (C----G)]. By using this approach, we have been able to define the mutation in 92.8% of cases. The rest (all but four) were defined by direct sequencing and this led to the detection of nine rare mutations [beta zero 76 (-C); beta+ IVSI nt 5 (G----A); beta+ IVSI nt 5 (G----C); beta+ IVSI -1 (cod 30) (G----C); beta+ -87 (C----T), beta zero -290 bp del.; beta+ -101 (C----T)], and to the characterization of a novel mutation consisting of the deletion of the G at the invariant AG of the IVSII splice acceptor site of the beta-globin gene (beta IVSII nt 850 -1 bp). In the remaining four cases, the beta-globin gene showed entirely normal sequences and the beta-globin gene cluster was intact, as indicated by Southern blot analysis. Fetal diagnosis was carried out by dot blot analysis with the oligonucleotide probes defined in the parents. The procedure is simple and reliable, and the results can be obtained within 1 week of sampling. No misdiagnosis has so far occurred. The results indicate that fetal diagnosis of beta-thalassemia by DNA analysis may be obtained in practically all cases (even in a population showing marked heterogeneity of beta-thalassemia) by the combination of dot blot analysis for detecting common mutations, and direct sequencing for defining those that are uncommon.
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