Beach nourishment using sediments from relict sand deposit: Effects on subtidal macrobenthic communities in the Central Adriatic Sea (Eastern Mediterranean Sea-Italy).

Nowadays nourishment is the most popular shore reconstruction strategy to counteract erosion of coastal areas. Sediments used for nourishment can have terrestrial or marine origin. This study analysed the effects of nourishment with relict sand on the subtidal macrobenthic communities and on the surface sediment at 7 sites of the Marche Region (Central Adriatic Sea, Italy). Samples for biological and physical analyses were collected in each site before and after nourishment. One year after nourishment the presence of the relict sands used for the replenishment is still visible in the sediment of each site. In the same period macrobenthic communities are characterised by the dominance of a few species able to avoid burial and suffocation phenomena, showing a low variability respect to the communities present before.

The "one-out, all-out" principle entails the risk of imposing unnecessary restoration costs: a study case in two Mediterranean coastal lakes.

The Water Framework Directive uses the "one-out, all-out" principle in assessing water bodies (i.e., the worst status of the elements used in the assessment determines the final status of the water body). In this study, we assessed the ecological status of two coastal lakes in Italy. Indices for all biological quality elements used in transitional waters from the Italian legislation and other European countries were employed and compared. Based on our analyses, the two lakes require restoration, despite the lush harbor seagrass beds, articulated macrobenthic communities and rich fish fauna. The "one-out, all-out" principle tends to inflate Type I errors, i.e., concludes that a water body is below the "good" status even if the water body actually has a "good" status. This may cause additional restoration costs where they are not necessarily needed. The results from this study strongly support the need for alternative approaches to the "one-out, all-out" principle.

Does psychomotor retardation define a clinically relevant phenotype of unipolar depression?

BACKGROUND: The recognition and assessment of psychomotor retardation may have implications for better definition of the clinical phenotypes of depression. The aim of this study was to assess the clinical correlates of psychomotor retardation endorsed at any time during the patients' lifetime (LPR). METHODS: The study sample included 291 patients with non-psychotic major depressive disorder (MDD) participating in the clinical trial, "Depression: The Search for Treatment-Relevant Phenotypes." Psychomotor retardation was measured using a factor derived from the Mood Spectrum Self-Report (MOODS-SR) assessment. Using a pre-defined cut-off score on the lifetime psychomotor retardation (LPR) factor of the MOODS-SR, participants were classified into high and low scorers. Logistic regression analysis was used to evaluate the relationship between LPR and subthreshold bipolarity. RESULTS: Compared to low scorers, participants with high scores on the LPR factor had greater severity of depression and more bipolarity indicators. CONCLUSIONS: The MOODS-SR appears to be helpful to identify clinical phenotypes of unipolar depression and to highlight the usefulness of a lifetime approach to the assessment of psychopathology in the characterisation of patients with unipolar depression.

Chimeric plant virus particles as immunogens for inducing murine and human immune responses against human immunodeficiency virus type 1.

The high-yield expression of a neutralizing epitope from human immunodeficiency virus type 1 (HIV-1) on the surface of a plant virus and its immunogenicity are presented. The highly conserved ELDKWA epitope from glycoprotein (gp) 41 was expressed as an N-terminal translational fusion with the potato virus X (PVX) coat protein. The resulting chimeric virus particles (CVPs), purified and used to immunize mice intraperitoneally or intranasally, were able to elicit high levels of HIV-1-specific immunoglobulin G (IgG) and IgA antibodies. Furthermore, the human immune response to CVPs was studied with severe combined immunodeficient mice reconstituted with human peripheral blood lymphocytes (hu-PBL-SCID). hu-PBL-SCID mice immunized with CVP-pulsed autologous dendritic cells were able to mount a specific human primary antibody response against the gp41-derived epitope. Notably, sera from both normal and hu-PBL-SCID mice showed an anti-HIV-1-neutralizing activity. Thus, PVX-based CVPs carrying neutralizing epitopes can offer novel perspectives for the development of effective vaccines against HIV and, more generally, for the design of new vaccination strategies in humans.

Determination, diversification and multipotency of mammalian myogenic cells.

In amniotes, myogenic commitment appears to be dependent upon signaling from neural tube and dorsal ectoderm, that can be replaced by members of the Wnt family and by Sonic hedgehog. Once committed, myoblasts undergo different fates, in that they can differentiate immediately to form the myotome, or later to give rise to primary and secondary muscle fibers. With fiber maturation, satellite cells are first detected; these cells contribute to fiber growth and regeneration during post-natal life. We will describe recent data, mainly from our laboratory, that suggest a different origin for some of the cells that are incorporated into the muscle fibers during late development. We propose the possibility that these myogenic cells are derived from the vasculature, are multi-potent and become committed to myogenesis by local signaling, when ingressing a differentiating muscle tissue. The implications for fetal and perinatal development of the whole mesoderm will also be discussed.

Skeletal myogenic progenitors originating from embryonic dorsal aorta coexpress endothelial and myogenic markers and contribute to postnatal muscle growth and regeneration.

Skeletal muscle in vertebrates is derived from somites, epithelial structures of the paraxial mesoderm, yet many unrelated reports describe the occasional appearance of myogenic cells from tissues of nonsomite origin, suggesting either transdifferentiation or the persistence of a multipotent progenitor. Here, we show that clonable skeletal myogenic cells are present in the embryonic dorsal aorta of mouse embryos. This finding is based on a detailed clonal analysis of different tissue anlagen at various developmental stages. In vitro, these myogenic cells show the same morphology as satellite cells derived from adult skeletal muscle, and express a number of myogenic and endothelial markers. Surprisingly, the latter are also expressed by adult satellite cells. Furthermore, it is possible to clone myogenic cells from limbs of mutant c-Met-/- embryos, which lack appendicular muscles, but have a normal vascular system. Upon transplantation, aorta-derived myogenic cells participate in postnatal muscle growth and regeneration, and fuse with resident satellite cells.The potential of the vascular system to generate skeletal muscle cells may explain observations of nonsomite skeletal myogenesis and raises the possibility that a subset of satellite cells may derive from the vascular system.

High efficiency myogenic conversion of human fibroblasts by adenoviral vector-mediated MyoD gene transfer. An alternative strategy for ex vivo gene therapy of primary myopathies.

Ex vivo gene therapy of primary myopathies, based on autologous transplantation of genetically modified myogenic cells, is seriously limited by the number of primary myogenic cells that can be isolated, expanded, transduced, and reimplanted into the patient's muscles. We explored the possibility of using the MyoD gene to induce myogenic conversion of nonmuscle, primary cells in a quantitatively relevant fashion. Primary human and murine fibroblasts from skin, muscle, or bone marrow were infected by an E1-deleted adenoviral vector carrying a retroviral long terminal repeat-promoted MyoD cDNA. Expression of MyoD caused irreversible withdrawal from the cell cycle and myogenic differentiation in the majority (from 60 to 90%) of cultured fibroblasts, as defined by activation of muscle-specific genes, fusion into contractile myotubes, and appearance of ultrastructurally normal sarcomagenesis in culture. 24 h after adenoviral exposure, MyoD-converted cultures were injected into regenerating muscle of immunodeficient (severe combined immunodeficiency/beige) mice, where they gave rise to beta-galactosidase positive, centrally nucleated fibers expressing human myosin heavy chains. Fibers originating from converted fibroblasts were indistinguishable from those obtained by injection of control cultures of lacZ-transduced satellite cells. MyoD-converted murine fibroblasts participated to muscle regeneration also in immunocompetent, syngeneic mice. Although antibodies from these mice bound to adenoviral infected cells in vitro, no inflammatory infiltrate was present in the graft site throughout the 3-wk study period. These data support the feasibility of an alternative approach to gene therapy of primary myopathies, based on implantation of large numbers of genetically modified primary fibroblasts massively converted to myogenesis by adenoviral delivery of MyoD ex vivo.

The high prevalence of "soft" bipolar (II) features in atypical depression.

Seventy-two percent of 86 major depressive patients with atypical features as defined by the DSM-IV and evaluated systematically were found to meet our criteria for bipolar II and related "soft" bipolar disorders; nearly 60% had antecedent cyclothymic or hyperthymic temperaments. The family history for bipolar disorder validated these clinical findings. Even if we limit the diagnosis of bipolar II to the official DSM-IV threshold of 4 days of hypomania, 32.6% of atypical depressives in our sample would meet this conservative threshold, a rate that is three times higher than the estimates of bipolarity among atypical depressives in the literature. By definition, mood reactivity was present in all patients, while interpersonal sensitivity occurred in 94%. Lifetime comorbidity rates were as follows: social phobia 30%, body dysmorphic disorder 42%, obsessive-compulsive disorder 20%, and panic disorder (agoraphobia) 64%. Both cluster A (anxious personality) and cluster B (e.g., borderline and histrionic) personality disorders were highly prevalent. These data suggest that the "atypicality" of depression is favored by affective temperamental dysregulation and anxiety comorbidity, clinically manifesting in a mood disorder subtype that is preponderantly in the realm of bipolar II. In the present sample, only 28% were strictly unipolar and characterized by avoidant and social phobic features, without histrionic traits.

A temperature-conditional mutant of simian virus 40 large T antigen requires serum to inhibit myogenesis and does not induce DNA synthesis in myotubes.

The temperature-conditional mutant tsA58 of SV40 large T antigen (Tag) increases the proliferation rate and the number of cell divisions in primary murine and human myogenic cells when expressed under permissive conditions (i.e., at 33 degrees C in medium containing high levels of serum). Under these conditions, Tag also prevents terminal differentiation. Under nonpermissive conditions (i.e., at 39 degrees C in medium containing low levels of serum) in which Tag is largely inactive, proliferation is arrested, and differentiation occurs. However, even at a permissive temperature, the removal of serum induced myosin expression and the fusion of myogenic cells, which continued to express functional Tag. Although Tag was complexed with pRb, as expected from a functional protein, proliferation was nevertheless arrested, and differentiation was induced. Consistent with these findings, the exposure of Tag-expressing differentiated myotubes to serum at 33 degrees C did not reinduce DNA synthesis in these cells. Thus, in myogenic cells, temperature-conditional mutants of Tag stimulate proliferation in the presence of serum but neither prevent terminal differentiation in the absence of serum nor induce DNA synthesis once complete withdrawal from the cycle has occurred.

Myogenic conversion of mammalian fibroblasts induced by differentiating muscle cells.

Somite-derived skeletal myoblasts are supposed to be the sole source of muscle fibre nuclei during pre- and postnatal development, but evidence is accumulating for unorthodox contributions to muscle fibre nuclei from other cell types. For example, in tissue culture, fibroblasts can fuse with dysgenic myoblasts and restore correct membrane function. We report here the results of a series of experiments investigating this phenomenon and its possible mechanism. 10T1/2 cells, infected with a replication defective retrovirus encoding the bacterial enzyme beta-galactosidase, fused to form beta-galactosidase positive, differentiated myotubes when cocultured with differentiating uninfected C2C12 or primary myogenic cells, but this did not occur when they were cocultured with other cells such as 3T3 fibroblasts or PC12 pheochromocytoma cells. Myogenic conversion ranged from 1 to 10% of the 10T1/2 cell population and required close cell interaction between the different cells types: it was not induced by conditioned medium or extracellular matrix deposited by C2C12 cells. Myogenic conversion was also observed in vivo, after injection of similarly infected 10T1/2 cells into regenerating muscle. Conversion was seen also after coculture of uninfected 10T1/2 cells with primary chick myoblasts, thus demonstrating that it was not dependent upon viral infection and that there is no species or class barrier in this phenomenon. Primary fibroblasts, isolated from different organs of transgenic mice carrying a Lac Z marker under the control of a muscle-specific promoter, restricting beta-galactosidase expression to striated muscle cells, also underwent myogenic conversion, when cocultured with C2C12 myoblasts.(ABSTRACT TRUNCATED AT 250 WORDS)