Anatomy and anatomists in Tuscany in the 17th century.

The 17th century was characterized by a real revolution in the field of scientific research due to the introduction of the experimental method, promoted by Galileo Galilei who was the most representative scientist of this period. Therefore, medical disciplines, particularly Anatomy, underwent innovative and deep changes shattering traditional culture and representing the background for the modern science. In this fermenting period, Tuscany played a significant role since numerous distinguished scientists were gathered by Medici Grand Dukes (especially Ferdinando the 2nd and Cosimo the 3rd) at Pisa University and at their court in Florence. Among them, it must be mentioned Giovanni Alfonso Borelli, creator of iathromechanics, Marcello Malpighi, founder of microscopic Anatomy, Francesco Redi, who denied the insect spontaneous generation, Nils Steensen who continued in Florence his anatomical studies on lymph nodes and salivary glands while setting also the bases of modern geology. Moreover, at the end of the 17th century, the anatomical wax modelling techniques arose and developed in Florence thanks to the work of Gaetano Zumbo (or Zummo), capable of creating some real masterpieces, still very well preserved and collected in the Museum of Natural Sciences "La Specola".

Bodies of stone: Girolamo Segato (1792-1836).

The life, activity and specimens of Girolamo Segato (Sospirolo 1792--Firenze 1836), as well as the mystery still surrounding his petrifaction method are outlined in this paper with the aim of shedding some light on one of the most controversial naturalists of the 19th century. Even if after his death many preparations became scattered or even destroyed, the greatest nucleus of them is now collected and exhibited in the Museum of the Department of Anatomy in Florence. Special attention has been given to the description of one of the most famous "pieces", a female head, recently added to the collection, coming from Museo Civico of Belluno. This sample, submitted to conventional Rx analysis and CT Scan Tomography, displays an outstanding injection of the thinnest peripheral blood vessels.

Morphofunctional integration between skeletal myoblasts and adult cardiomyocytes in coculture is favored by direct cell-cell contacts and relaxin treatment.

The success of cellular cardiomyoplasty, a novel therapy for the repair of postischemic myocardium, depends on the anatomical integration of the engrafted cells with the resident cardiomyocytes. Our aim was to investigate the interaction between undifferentiated mouse skeletal myoblasts (C2C12 cells) and adult rat ventricular cardiomyocytes in an in vitro coculture model. Connexin43 (Cx43) expression, Lucifer yellow microinjection, Ca2+ transient propagation, and electrophysiological analysis demonstrated that myoblasts and cardiomyocytes were coupled by functional gap junctions. We also showed that cardiomyocytes upregulated gap junctional communication and expression of Cx43 in myoblasts. This effect required direct cell-to-cell contact between the two cell types and was potentiated by treatment with relaxin, a cardiotropic hormone with potential effects on cardiac development. Analysis of the gating properties of gap junctions by dual cell patch clamping showed that the copresence of cardiomyocytes in the cultures significantly increased the transjunctional current and conductance between myoblasts. Relaxin enhanced this effect in both the myoblast-myoblast and myoblast-cardiomyocyte cell pairs, likely acting not only on gap junction formation but also on the electrical properties of the preexisting channels. Our findings suggest that myoblasts and cardiomyocytes interact actively through gap junctions and that relaxin potentiates the intercellular coupling. A potential role for gap junctional communication in favoring the intercellular exchange of regulatory molecules, including Ca2+, in the modulation of myoblast differentiation is discussed.

The oligosaccharidic content of the glycoconjugates of the prepubertal descended and undescended testis: lectin histochemical study.

The saccharidic content of the glycoconjugates has been studied in the descended the undescended testes of a 8 years old boy. For this purpose, a battery of seven HRP-conjugated lectins (SBA, DBA,PNA,WGA,UEAI, LTA and ConA) was used. D-galactose-N-acetyl-D-galactosamine and alpha-L-fucose sugar residues, which were present in the cytoplasm of the Sertoli cells of the normally positioned prepubertal testis, were not detected in the same cells of the undescended testis. The Leydig's cells of the descended testis appeared characterized by N-acetyl-D-glucosamine which was absent in the rare and atrophic Leydig's cells of the cryptorchid testis. Differences in sugar residues distribution between the descended and the undescended testis were also detected in the lamina propria of the seminiferous tubules. Peritubular myoid cells in the undescended testis only reacted with PNA, after neuraminidase digestion, thus revealing the presence of D-galactose (beta1-->3)-N-acetyl-D-galactosamine and sialic acid. In this study a complete distributional map of the sugar residues of the glycoconjugates in the descended and undescended prepubertal testis is reported.

Apoptosis shifts to necrosis via intermediate types of cell death by a mechanism depending on c-myc and bcl-2 expression.

Hypoxic and chemical hypoxia (antimycin A) commits cultured rat fibroblasts (Rat-1) towards apoptosis, necrosis or an intermediate form of cell death (aponecrosis) depending on the degree of hypoxia. Aponecrosis also occurs in vivo. Here, we demonstrate that c-myc and bcl-2, two proto-oncogenes known to lower or to enhance, respectively, the apoptotic threshold, also affect the type of cell death: apoptosis shifts to aponecrosis and aponecrosis to necrosis, depending on c-myc or bcl-2 expression and the antimycin A concentration (100-400 microM). In cells with basal gene expression, apoptosis shifts to aponecrosis/necrosis at 300 microM antimycin A (middle hypoxia). Overexpression of c-myc markedly increases cumulative cell death in response to antimycin A and lowers the antimycin A concentration required to shift apoptosis to aponecrosis/necrosis from 300 microM to 100 microM (low hypoxia). Overexpression of bcl-2 elicits the opposite effect, decreasing cumulative cell death in response to antimycin A and raising the drug concentration required to shift apoptosis to aponecrosis/necrosis to 400 microM (high hypoxia). The passage from one to the other form of cell death involves various aponecrotic features with observed intermediate aspects between apoptosis and necrosis, a progressive increase in necrotic features being correlated with an increase in antimycin A concentration. The mechanism underlying the various effects of c-myc and bcl-2 on cell-death type has been related to the ability of these genes to counteract, to various extents, the ATP decrease occurring in response to different degrees of chemical hypoxia.