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Il testo espone i principi generali che governano il funzionamento delle cellule, approfondisce l’anatomia dei genomi, i meccanismi molecolari e le regolazioni presenti alla base della trascrizione, della traduzione, della replicazione e manutenzione dell’informazione genetica. Riporta inoltre alcuni esempi di differenziamento, di utilizzo specifico e finemente regolato di parti cruciali dell’informazione genetica. Nuovi paragrafi e nuovi inserti dedicati in particolare alle tecniche di indagine, dalle classiche a quelle più avanzate, vanno a completare la discussione delle diverse tematiche.

The essential requirement for a successful myocardial tissue engineering is that scaffolds and tissue constructs exhibit biomimetic activity toward cells. Our aim was to investigate the significance of cell-matrix interactions in cardiac tissue microenvironment in vitro. Cardiac fibroblasts from normal (CF-N) and pathological (CF-P) hearts with ischemic cardiopathy deposited extracellular matrix (Mx) and conditioned medium (Cm), which were then characterized by immunohistology, immunoblotting, ELISA-based protein array or mass spectrometry. Normal and pathological cardiac primitive cells CPC-N and -P) were cultured on CF-Mx-N and -P or in CF-Cm-N and -P and their proliferation, apoptosis, migration and maturation were evaluated by BrdU, TdT, scratch wound assays or RT-PCR, respectively. Laminin-1 and tenascin-X were detected in CF-Mx-P. The expression of IGFBP1, Il-6, EGF was higher in CF-Cm-P, while that of SCF, TGF-?3, BMP4 was higher in CF-Cm-N. Migration speed of CPC-P peaked at 21.3 ?m/h on CF-Mx-N. Proliferation of CPCs increased significantly on CF-Mx-P, while apoptosis diminished on both types of matrix. In CPC-N, maturation toward cardiomyocytes was activated by CF Mx-N and toward endothelial cells by CF-Mx-P; in CPC-P the trend toward smooth muscle cell-lineage was evident on both substrates. CF-Cm-N reduced apoptosis of CPC-N (2-fold), while CF-Cm-P reduced apoptosis of CPC-P (3.5-fold) and increased proliferation of CPC-N (1.6-fold, n=3, p

Direct product convolutional codes are the result of a special concatenated scheme based on the well-known method of direct product for combining block codes. The approach taken for its construction is to consider convolutional codes as block codes over the field of rational functions F(D). This relatively new codes has been previously defined and investigated by the author, but in this instance, further properties and aspects about the product convolutional codes are considered. The new aspects studied are: some properties and physical realization of encoders, considerations on convergence of decoding based on EXIT charts and the effect of the blocking factor on BER performance in AWGN channel. In addition, the construction of multidimensional product convolutional codes is considered.

The beta-amyloid peptide (Abeta) present in the senile plaques of Alzheimer's disease derives from the cleavage of a membrane protein, named APP, driven by two enzymes, known as beta- and gamma-secretases. The mechanisms regulating this cleavage are not understood. We have developed an experimental system to identify possible extracellular signals able to trigger the cleavage of an APP-Gal4 fusion protein, which is detected by measuring the expression of the CAT gene transcribed under the control of the Gal4 transcription factor, which is released from the membrane upon the cleavage of APP-Gal4. By using this assay, we purified a protein contained in the C6 cell-conditioned medium, which activates the cleavage of APP-Gal4 and which we demonstrated to be PDGF-BB. The APP-Gal4 processing induced by PDGF is dependent on the gamma-secretase activity, being abolished by an inhibitor of this enzyme, and is the consequence of the activation of a pathway downstream of the PDGF-receptor, which includes the non-receptor tyrosine kinase Src and the small G-protein Rac1. These findings are confirmed by the observation that a constitutively active form of Src increases Abeta generation and that, in cells stably expressing APP, the generation of A is strongly decreased by the Src tyrosine kinase inhibitor PP2.

Background Celiac disease is an inflammatory condition of the small intestine that affects genetically predisposed individuals after dietary wheat gliadin ingestion. Type 2-transglutaminase (TG2) activity seems to be responsible for a strong autoimmune response in celiac disease, TG2 being the main autoantigen. Several studies support the concept that celiac anti-TG2 antibodies may contribute to disease pathogenesis. Our recent findings on the ability of anti-TG2 antibodies to induce a rapid intracellular mobilization of calcium ions, as well as extracellular signal-regulated kinase phosphorylation, suggest that they potentially act as signaling molecules. In line with this concept, we have investigated whether anti-TG2 antibodies can induce phosphoproteome modification in an intestinal epithelial cell line. Methods and Principal Findings We studied phosphoproteome modification in Caco-2 cells treated with recombinant celiac anti-TG2 antibodies. We performed a two-dimensional electrophoresis followed by specific staining of phosphoproteins and mass spectrometry analysis of differentially phosphorylated proteins. Of 14 identified proteins (excluding two uncharacterized proteins), three were hypophosphorylated and nine were hyperphosphorylated. Bioinformatics analyses confirmed the presence of phosphorylation sites in all the identified proteins and highlighted their involvement in several fundamental biological processes, such as cell cycle progression, cell stress response, cytoskeletal organization and apoptosis. Conclusions Identification of differentially phosphorylated proteins downstream of TG2-antibody stimulation suggests that in Caco-2 cells these antibodies perturb cell homeostasis by behaving as signaling molecules. We hypothesize that anti-TG2 autoantibodies may destabilize the integrity of the intestinal mucosa in celiac individuals, thus contributing to celiac disease establishment and progression. Since several proteins here identified in this study were already known as TG2 substrates, we can also suppose that transamidating activity and differential phosphorylation of the same targets may represent a novel regulatory mechanism whose relevance in celiac disease pathogenesis is still unexplored.

Objetivo: Identificar factores predictivos de éxito después de una sesión única de litotricia extracorpórea por ondas de choque (LEOC) a las tres semanas de seguimiento. Material y métodos: Se revisaron los registros clínicos de 116 pacientes con cálculos urinarios únicos sometidos a LEOC entre octubre 2007 y agosto 2009. Las tomografías axiales computarizadas preoperatorias de todos los pacientes fueron revisadas por dos radiólogos en desconocimiento del desenlace clínico. El éxito fue definido como la desaparición completa del cálculo o la persistencia de fragmentos < 2mm en la radiografía simple realizada durante las tres primeras semanas de seguimiento. El impacto de factores clínicos y radiológicos fue evaluado utilizando regresión logística. Resultados: La tasa de éxito de LEOC a las tres semanas de seguimiento fue del 49,1%. Tamaño < 8mm, área del cálculo < 30 mm², localización en el uréter distal, densidad < 1.000 UH y fragmentación intraoperatoria demostraron una significativa asociación con éxito en el análisis univariado (p

RESUMENObjetivo. Evaluar el efecto de la ingestión de lípidos durante períodos cortos (20 días) ylargos (90 días) sobre la actividad hepática y en tracto gastrointestinal (TGI) de las enzimascatalasa (CAT), superóxido dismutasa (SOD) y glutatión peroxidasa (GPx). Materiales ymétodos. Se utilizó el Índice peróxidos (VP) y el índice anisidina (VA) para detectar lapresencia de productos de la oxidación en las raciones. Se realizó un análisis de varianzabajo un modelo de parcelas divididas en el tiempo. Cuando se encontraron diferencias(p

Objetivo. Evaluar el efecto de la ingestión de lípidos durante períodos cortos (20 días) y largos (90 días) sobre la actividad hepática y en tracto gastrointestinal (TGI) de las enzimas catalasa (CAT), superóxido dismutasa (SOD) y glutatión peroxidasa (GPx). Materiales y métodos. Se utilizó el índice peróxidos (VP) y el índice anisidina (VA) para detectar la presencia de productos de la oxidación en las raciones. Se realizó un análisis de varianza bajo un modelo de parcelas divididas en el tiempo. Cuando se encontraron diferencias (p0.95), suggesting that GIT-GPx activity is a good indicator of the lipid oxidative status of rations.