Measurement of gap between abutment and fixture in dental conical connection implants. A focused ion beam SEM observation.

BACKGROUND: The aim of the authors was to examine the abutment-fixture interface in Morse-type conical implants in order to verify gaps at this level using a new microscopical approach. MATERIAL AND METHODS: In this in vitro study, 20 abutment-fixture complexes were prepared by sectioning (longitudinal and cross-sectional to the long axis) with a microtome and then with a focused ion beam (FIB). This is a micrometric machine tool that uses gallium ions to abrade circumscribed areas to dig deeper into the cuts obtained with the microtome in order to eliminate cut-induced artifacts. This is because the FIB abrasion is practically free from artifacts, which are normally generated by the action of the microtome blades or other techniques. Samples were then observed by scanning electron microscopy (SEM). RESULTS: The observation of the abraded parts with the FIB permitted measurement of the real gap between the implant-abutment components. A variable amount of gap was retrieved (from 0 to 3 µm) by the observations, confirming the non-hermetic nature of the connection. It has to be pointed out that in approximately 65% of cases, the gap accounted for less than 1 µm. CONCLUSIONS: The reported data confirmed that the analyzed connection system allowed for minimal gap. However, from the evidence of the present analysis, it cannot be assumed that the 2 parts of a Morse-type conical implant are fused in 1 piece, which would create a perfectly matched hermetic connection.

Differential expression of laminin isoform (alpha2), integrins (alpha3beta1 and alpha6beta4) and cytokeratin 20 in H. pylori gastritis.

The expression of laminin-1 chains (beta1 and gamma1), laminin-2 (merosin), integrin receptors to laminin (alpha3beta1 and alpha6beta4) and cytokeratin (CK20) were studied by immunohistochemical methods in gastric biopsies from antrum of 25 patients. H. pylori gastritis was found in 19 cases and intestinal metaplasia (IM) in four from these 19. Another 13 biopsies, all with IM were immunostained to laminin-2. Laminin-1 chains in normal and gastritis areas without IM were expressed as a strong, linear and continuous deposit in the basement membranes of the superficial and glandular epithelium. In metaplastic glands the reactivity to laminin-1 chains was decreased. Merosin was discontinuous when a moderate to accentuated H. pylori glandular colonization was present. Samples with IM were negative to laminin-2. The alpha3beta1 and alpha6beta4 integrins were negative only in IM gastric biopsies. The CK20 immunoreactivity was strong and homogeneous in the cells at the tip and the upper portion of foveolae in normal areas and in gastritis with IM the reactivity to CK 20 was heterogeneous. A differential expression of laminin isoforms is related to inflammation and subsequent IM caused by H. pylori. The alterations of alpha3beta1 and alpha6beta4 parallel both modifications in merosin and CK20 expression in H. pylori chronic gastritis.

[The histopathological and microbiological aspects in a model of acute acalculous cholecystitis: an experimental study]. / Aspetti istopatologici e microbiologici in un modello di colecistite acuta alitiasica: studio sperimentale.

The early stages of acute acalculous cholecystitis (ACC) have been difficult to investigate due to the animal models developed and utilized over the past years. A new model of animal AAC induced by intra-abdominal sepsis is presented. Under general anesthesia 35 guinea pigs underwent laparotomy. The designed model included ligation and prick of the caecum in 25 animals (group A), while 10 animals served as control group (group B). Seven days after these experimental procedures animals underwent relaparotomy and were submitted to cholecystectomy and sacrifice. Histological studies of the specimen revealed various degrees of cholecystitis in all the gallbladders of survived animals from group A. Gallbladders of animals from group B were histologically normal. Gallbladder bile of 15 survived animals from group A were cultured. Bile cultures were negative in 10, while culture of gallbladder bile were positive in 5; the pathogen cultured were Streptococcus Faecalis and Streptococcus Sp. The results of this study suggest that intra-abdominal sepsis induces gallbladder inflammation of various degrees. This directly supports the theoretical relationship indicating that sepsis and shock could produce AAC. Moreover this model proved that AAC, in early stages, is primarily induced by inflammatory processes, while infection of the bile do represent a late event.

Inhibition of the oncogene product p185erbB-2 in vitro and in vivo by geldanamycin and dihydrogeldanamycin derivatives.

The erbB-2 oncogene encodes a transmembrane protein tyrosine kinase which plays a pivotal role in signal transduction and has been implicated when overexpressed in breast, ovarian, and gastric cancers. Naturally occurring benzoquinoid ansamycin antibiotics herbimycin A, geldanamycin (GDM), and dihydrogeldanamycin were found to potently deplete p185, the erbB-2 oncoprotein, in human breast cancer SKBR-3 cells in culture. Chemistry efforts to modify selectively the quinoid moiety of GDM afforded derivatives with greater potency in vitro and in vivo. Analogs demonstrated inhibition of p185 phosphotyrosine in cell culture and in vivo after systemic drug administration to nu/nu nude mice bearing Fisher rat embryo cells transfected with human erbB-2 (FRE/erbB-2). Specifically, dosed intraperitoneally at 100 mg/kg, 17-(allylamino)-17-demethoxygeldanamycin and other 17-amino analogs were effective at reducing p185 phosphotyrosine in subcutaneous flank FRE/erbB-2 tumors. Modifications to the 17-19-positions of the quinone ring revealed a broad structure-activity relationship in vitro.

erbB-2 oncogene inhibition by geldanamycin derivatives: synthesis, mechanism of action, and structure-activity relationships.

Overexpression of the erbB-2 oncogene has been linked to poor prognosis in breast, ovarian, and gastric cancers. Naturally occurring benzoquinoid ansamycin antibiotics herbimycin A, geldanamycin (GDM), and dihydrogeldanamycin were found to potently deplete p185, the erbB-2 oncoprotein, in human breast cancer SKBR-3 cells in culture. Chemistry efforts to modify selectively the ansa ring of GDM afforded derivatives with greater potency in vitro and in vivo. Analogs demonstrated inhibition of p185 phosphotyrosine in cell culture and in vivo after systemic drug administration to nu/nu nude mice bearing Fisher rat embryo cells transfected with human erbB-2. Functional group modification in the ansa ring was performed stereoselectively and regiospecifically without the need for protection strategies. Essential functional groups that were required for anti-erbB-2 activity were the 7-carbamate and the 2,3-double bond. Modification of the functional groups at the other positions was permitted. Structure-activity relationships are described for 1-5-, 7-9-, 11-, 15-, and 22-substituted geldanamycins.