Graphitic carbon in a nanostructured titanium oxycarbide thin film to improve implant osseointegration.

A nanostructured coating layer on titanium implants, able to improve their integration into bones and to protect against the harsh conditions of body fluids, was obtained by Ion Plating Plasma Assisted, a method suitable for industrial applications. A titanium carbide target was attached under vacuum to a magnetron sputtering source powered with a direct current in the 500-1100 W range, and a 100 W radio frequency was applied to the sample holder. The samples produced at 900 W gave the best biological response in terms of overexpression of some genes of proteins involved in bone turnover. We report the characterization of a reference and of an implant sample, both obtained at 900 W. Different micro/nanoscopic techniques evidenced the morphology of the substrates, and X-ray Photoelectron Spectroscopy was used to disclose the surface composition. The layer is a 500 nm thick hard nanostructure, composed of 60% graphitic carbon clustered with 15% TiC and 25% Ti oxides.

Lamellar body formation in normal and surfactant protein B-deficient fetal mice.

Surfactant protein B (SP-B) -/- mice die of lethal respiratory distress syndrome shortly after birth. Alveolar type II epithelial cells in SP-B-deficient mice are characterized by a complete absence of lamellar bodies, the intracellular storage form of pulmonary surfactant, and the presence of inclusions containing numerous small vesicles and electron-dense masses. The present study was undertaken to characterize the formation of these inclusions during fetal lung development and clarify their relationship to lamellar bodies. In wild-type and SP-B +/- mice, small lamellar bodies with loosely organized lamellae and distinct limiting membranes were first detected on day 16 to 16.5 of gestation. SP-B -/- mice were readily identified on day 16 by the absence of immature lamellar bodies, the appearance of vesicular inclusions similar to those previously described in late gestation SP-B -/- mice, and the accumulation of misprocessed SP-C protein. Vesicular inclusions were rarely detected in SP-B +/- mice and were never detected in wild-type littermates. Classical multivesicular bodies were observed fusing with lamellar bodies in wild-type mice, and with the vesicular inclusions in SP-B -/- mice that occasionally contained a few membrane lamellae. On day 18, the airways of SP-B -/- mice lacked tubular myelin and were filled with vesicles and electron-dense masses, suggesting that the contents of the vesicular inclusions were secreted. Taken together, these observations suggest that vesicular inclusions in SP-B -/- mice are disorganized lamellar bodies in which the absence of SP-B leads to failure to package surfactant phospholipids into concentric lamellae.

The testis isoform of the phosphorylase kinase catalytic subunit (PhK-gammaT) plays a critical role in regulation of glycogen mobilization in developing lung.

In order to identify the form of phosphorylase kinase catalytic subunit expressed in developing lung, degenerate polymerase chain reaction primers were designed based on conserved domains of the two known catalytic subunits, expressed primarily in muscle and testis. Amplification of cDNA from day 19 fetal rat lung followed by cloning and sequence analyses indicated that only the testis isoform of phosphorylase kinase (PhK-gammaT) was detectable in fetal lung. In situ hybridization analyses indicated that expression of PhK-gammaT RNA in developing lung tissue was widespread and not restricted to Type II epithelial cells; PhK-gammaT protein expression was temporally and spatially correlated with expression of PhK-gammaT RNA. PhK-gammaT RNA and protein expression was also characterized in the PhK-deficient glycogen storage disease (gsd) rat. PhK-gammaT RNA levels were similar in Type II cells isolated from wild type and gsd/gsd fetuses; in contrast, PhK-gammaT protein was virtually undetectable in gsd/ gsd Type II cells and enzyme activity was very low. These results suggest that PhK-gammaT plays a critical role in mobilization of glycogen during fetal lung development and that failure to catabolize glycogen in the gsd/gsd rat is related to an untranslatable PhK-gammaT RNA or unstable protein.

Long-term treatment with rifaximin and lactobacilli in post-diverticulitic stenoses of the colon.

The authors report their endoscopic experience in the treatment of intestinal inflammatory complications and their prevention with cyclic antibiotic treatment (rifaximin 400 mg b.i.d. for 7 days/month), followed by recolonizing treatment with lactobacilli (2 capsules in the morning for 7 days/month), for an overall period of 12 months. In all 79 cases (45 males and 34 females, mean age 63 years, range 55-75 years), the treatment proved capable of controlling the symptoms and averting the onset of the complications which follow attacks of acute diverticulitis. These complications include uncontrollable sepsis, free perforation of a hollow viscus, evolutive fistulation, intestinal occlusion, abscesses not drained percutaneously, all factors which necessitate urgent elective surgery. Rifaximin, together with lactobacillus treatment, proved to be effective, well-tolerated and safe, and can thus be considered an indispensable aid in the treatment of diverticular disease and in the prevention of its complications.

A modification of an affinity procedure for purification of human C1- inhibitor that provides a homogeneous stable preparation.

Human C1- inhibitor can be rapidly purified by the affinity chromatography procedure described by Pilatte and his associates (1989), but the inhibitor so purified breaks down during storage or is in a cleaved form when initially purified. By adding an ion-exchange chromatography procedure after the affinity chromatography, a stable, single species of C1- inhibitor molecules is obtained. It is likely that serine proteinases in trace amounts, which may be complexed with some of the C1- inhibitor, are removed during the ion-exchange procedure. This procedure provides a highly purified and useful preparation of C1- inhibitor.