Incidence of anterior disc displacement without reduction of the temporomandibular joint in patients with dentofacial deformity.

The aim of this study was to investigate the incidence of anterior disc displacement without reduction (ADDwoR) of the temporomandibular joint (TMJ) in patients with dentofacial deformity. Eighty-eight female patients (176 joints) with skeletal class III malocclusion and 33 female patients (66 joints) with skeletal class II malocclusion, with or without anterior open bite and asymmetry, were evaluated. Magnetic resonance imaging (MRI) of the TMJ was used to diagnose ADDwoR. A statistical analysis was performed to examine the relationship between ADDwoR and skeletal structure. ADDwoR was present in 37 of the 66 joints (56.1%) in class II compared to 34 of the 176 joints (19.3%) in class III (P<0.05). In class III, ADDwoR was significantly more common in joints with mandibular asymmetry (24/74; 32.4%) than in joints with open bite (9/62; 14.5%) and joints with open bite and without mandibular asymmetry (1/38; 2.6%). In class II, ADDwoR was significantly less common in joints with mandibular asymmetry and without open bite (1/8; 12.5%). ADDwoR was only observed on the deviated side in both class III and class II with mandibular asymmetry. The prevalence of ADDwoR differed according to the dentofacial morphology.

Single-nucleus polycrystallization in thin film epitaxial growth.

We have observed, by use of low-energy electron microscopy, the first direct evidence of self-driven polycrystallization evolved from a single nucleus in the case of epitaxial pentacene growth on the Si(111)-H terminated surface. In this Letter we demonstrate that such polycrystallization can develop in anisotropic systems (in terms of crystal structure and/or the intermolecular interactions) when kinetic growth conditions force the alignment of the intrinsic preferential growth directions along the density gradient of diffusing molecules. This finding gives new insight into the crystallization of complex molecular systems, elucidating the importance of nanoscale control of the growth conditions.

Activation of the p21(Waf1/Cip1) promoter by the ets oncogene family transcription factor E1AF.

p21(Waf1/Cip1) is one of the key regulatory proteins in cell cycle, terminal differentiation, and apoptosis. Its promoter was shown to be transactivated by the wild-type p53 protein as well as in a p53-independent manner. In this report, we demonstrate that E1AF, an ets-related transcription factor, activates the human p21(Waf1/Cip1) promoter by interacting with the ets-binding sites located close to the two previously identified p53-responsive elements. Northern blot analysis revealed that p21(Waf1/Cip1) and E1AF were correlatively upregulated in response to cisplatin treatment in SiHa cells. Transient expression assays demonstrated that E1AF can activate the p21(Waf1/Cip1) promoter-driven luciferase reporter gene in SiHa cells. The p21(Waf1/Cip1) promoter activity was also increased in p53-null Saos2 osteosarcoma cells, but was markedly reduced when the ets-binding sites were deleted. These results indicate that E1AF positively regulates transcription from the p21(Waf1/Cip1) promoter in response to genotoxic stresses.

Streptozotocin diabetes: prolonged inflammatory response with delay in granuloma formation.

Inflammatory responses to carrageenin in streptozotocin-induced diabetic rats proved to be characterized by low values of granuloma tissue (tissue) weight and granuloma pouch fluid (fluid) volume, high values of fluid beta-glucuronidase (beta-Gl) and leucine aminopeptidase (LAP), and furthermore by high values of fluid lipid peroxide (LPO) and lactate dehydrogenase (LDH) and low values of fluid proamidase. These results in such diabetic rats were similar to those in rats injected with high doses of carrageenin except tissue weight and fluid volume. On the basis of measurements of three basic parameters required for coordinated observation of the inflammatory system, namely lysosomal enzymes, LPO, and proamidase (related respectively to the inflammatory response sensu stricto, to tissue damage, and to tissue repair), it can be concluded that the diabetic rats show an inadequately adapted inflammatory response, with decreased granuloma formation and reduced exudation, to noxious agents. This is probably due to a low sensitivity of the inflamed tissue in diabetic rats to noxious stimuli or chemical mediators, leading to a delay in the normal defence reaction of enhanced granuloma formation and exudation, thus resulting in a prolonged inflammatory response with a delay in wound healing.